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生物细胞(英文)

生物细胞(英文)

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生物细胞(英文) >2023年第11期

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  • 摘要：This work aimed to investigate the synergetic therapeutic effects of polydeoxyribonucleotides(PDRN)combined with extracorporeal shock waves therapy(ESWT)and the effects of the therapy according to ESWT sequences on a chronic traumatic full-thickness rotator cuff tear(RCT)in rabbit models.For this purpose,thirty-two rabbits were randomly allocated into 4 groups.An excision was made to create a 5-mm sized full-thickness RCT right proximal to the insertion site on the supraspinatus.After 6 weeks,4 different procedures(normal saline,Group 1;PDRN injection,Group 2;PDRN injection before ESWT,Group 3;PDRN injection after ESWT,Group 4)were performed.PDRN injection and radial type ESWT were each performed 4 times per week.Gross morphology,Immunohistochemistry,and motion analysis were performed at 4 weeks after treatments.All parameters including tear size,Masson’s trichrome(MT)staining,anti-collagen 1 monoclonal antibody immunostaining(COL-1),proliferating cell nuclear antigen(PCNA),vascular endothelial growth factor(VEGF),anti-platelet endothelial cell adhesion molecule-1 polyclonal antibody(PECAM-1),and motion analysis,were significantly greater in Group 2,Group 3,and Group 4 than in Group 1.In Group 4,all parameters were significantly greater than in Group 2,and parameters including MT staining,COL-1,PCNA,PECAM-1,and fast walking time were significantly greater than Group 3.There were no significant differences between Group 2 and Group 3.This study demonstrated that PDRN injection alone and combined with ESWT were more effective than control treatment and applying ESWT before PDRN injection was also shown to yield better outcomes in parameters including angiogenesis,cell proliferation,and fast walking time in a rabbit model with chronic traumatic full-thickness RCT.Therefore,the application of ESWT before PDRN injection could be recommended for optimal outcomes of the conservative treatments when the patients with full-thickness RCT are not suitable in surgical treatment.
  • 摘要：In these times of despair when a nano-sized organism,the SARS-CoV-2,has rendered the human race helpless,made the global health status decline,and drowned the world economy,a ray of hope comes from another nano-sized particle,the exosome.The potential of mesenchymal stem cells has already been established in COVID-19;however,cell-based therapy has its risks.We thereby propose cell-free therapy using stem cells-derived exosomes to fight against COVID-19,as they can be a game-changer owing to their immunomodulatory nature,which combats the cytokine storm characterizing this disease,and their practical efficiency,which will realistically aid large access to therapy worldwide.
  • 摘要：Psoriasis is an autoimmune-related chronic inflammatory disease with an approximate prevalence of 2–3%around the world,involving increased keratinocyte proliferation.Indeed,Th17 cells and IL-17 play critical roles in the pathogenesis of psoriasis.The monoclonal antibodies against cytokines have been shown to have effectively immunosuppressive effects on human psoriasis.However,there are still some patients that have no response to these treatments.Some patients have even serious side-effects which may affect their life.Mesenchymal stem cells have the ability of immunosuppressive and anti-inflammatory effects,which may be an alternative therapy with more safety and efficacy for human psoriasis.Moreover,the underlying mechanisms by which the MSCs prevent or ameliorate psoriasis are still poorly understood.Here,we first isolated and characterized human adipose,placenta,and umbilical cord-derived mesenchymal stem cells(haMSCs,hpMSCs,and huMSCs).After that,the animal model of imiquimod(IMQ)-induced psoriasis in C57BL/6 mice was confirmed.We investigated the impact of haMSCs,hpMSCs,and huMSCs on this model by H&E staining,immunohistochemistry staining,and quantitative real-time PCR.Data analysis showed that mice subcutaneously injected with these MSCs had a significantly decreased epidermal thickness,which was caused by obviously reduced hyper-proliferation of keratinocytes.Furthermore,our findings revealed that the infiltration of T cells to psoriatic lesions in IMQ-induced psoriasis mice was markedly downregulated by intradermal administration of haMSCs,hpMSCs,and huMSCs,respectively.Consequently,the production of IL-17 from Th17 cells was reduced,which inhibits the proliferation of keratinocytes in lesioned skin of IMQ-induced psoriasis mice.These data suggest that haMSCs,hpMSCs,and huMSCs can inhibit the effects of proinflammatory Th17 cells on the development of psoriasis,which may be potential therapeutic candidates for skin inflammatory disease or other autoimmune diseases.
  • 摘要：Ovarian cancer was one of the most common malignant tumors in female reproductive organs.Moreover,epithelial ovarian cancer showed the highest mortality rate in gynecological tumors,posing serious threats to women’s life and health.Transient Receptor Potential Cation Channel Subfamily V Member 2(TRPV2)and matrix metalloproteinase-2 MMP-2 have been found to play important roles in regulating the pathogenesis of most tumors,but there were few studies exploring the relationships of TRPV2 and MMP-2 in OC.Therefore,we evaluated the expression of TRPV2 and MMP-2 proteins in cancer tissues and adjacent normal tissues of OC patients.Immunohistochemistry was used to analyze the expressions of TRPV2 and MMP-2 in cancer tissues(N=70)and adjacent normal tissues(N=70)of OC patients,and the correlation of TRPV2 and MMP-2 with the occurrence and development of OC was analyzed with the combination of clinicopathological parameters of OC patients.The results showed that the expressions of TRPV2 and MMP-2 in OC tissues were significantly higher than those in adjacent normal tissues,and there were significant differences in TRPV2 and MMP-2 expressions in terms of tumor stage,differentiation,and lymph node metastasis of OC.Taken together,our results showed that protein expressions of TRPV2 and MMP-2 were closely related associated with the occurrence and development of OC.
  • 摘要：This work aimed to discover new therapeutic targets in renal clear cell carcinoma by bioinformatics and detect the effect of candidate gene TRIP13 in renal cell carcinoma(RCC)cell proliferation,migration,and invasion.Differentially expressed mRNAs were screened based on The Cancer Genome Atlas(TCGA)-Kidney Renal Clear Cell Carcinoma(KIRC)databases,and functional enrichments,survival analysis,receiver operating characteristic curve(ROC),and Protein–Protein Interaction(PPI)protein interaction analysis were performed by R software to screen the candidate gene TRIP13.Then,the expression of candidate gene TRIP13 in 92 pairs of cancer and adjacent normal tissues of renal clear cell carcinoma patients were detected by qRT-PCR,western blotting,and immunochemical analysis.The TRIP13 level and clinicopathological characteristics of patients with renal clear cell carcinoma were analyzed.Using 186-O and ACHN RCC cell lines with TRIP13 overexpressing or downregulating,the effect of TRIP13 on cell viability and proliferation were detected by CCK8 and EdU staining,respectively.The migration and invasion were detected by Transwell assays.A total of 19858 differentially expressed genes,5823 differentially expressed genes,3657 up-regulated genes,and 2166 down-regulated genes were identified.TRIP13 was closed associated with cell cycle regulation,and survival and prognosis of renal clear cell carcinoma were selected as a candidate gene.The mRNA and protein levels of TRIP13 in cancer tissues were higher than that in adjacent normal tissues.TRIP13 level was significantly associated with tumor size,tumor stage,Fuhrman grade,and lymph node metastasis.TRIP13 overexpression significantly increased cell viability,proliferation,migration,and invasion,while downregulating of TRIP13 had opposite effects in both 186-O and ACHN cells.Therefore,TRIP13 promotes RCC proliferation and metastasis,which should be a novel biomarker for early diagnosis,treatment,and prognosis of RCC.
  • 摘要：This study aims to investigate the protective effects of peroxiredoxin 6 on the total motility and progressive motility of human spermatozoa.Semen samples with normal parameters were collected from 23 males and supplemented with different concentrations of peroxiredoxin 6.All the semen samples were measured according to the WHO 5th manual,and the motile spermatozoa were extracted using IVF fertilization medium supplemented with different peroxiredoxin 6 concentrations.Total motility and progressive motility were observed at different time-points of culture at room temperature.After peroxiredoxin 6 supplementation,all groups had a significant increase in total motility and progressive motility compared to the control group.The difference in total motility and progressive motility between the 0 and 10−7 mM groups was observed at 24 and 48 h of culture at room temperature.At 24 h,the total motility increased by 30%in the control group(16.03±11.91 vs.11.51±7.84),and progressive motility increased by 21%(10.53±9.4 vs.8.31±6.04).A similar trend was observed in the 48 h group.In addition,we also found that peroxiredoxin 6 had a well protective effect on sperm kinetic parameters at 10−7 mM.The findings of this study suggest that peroxiredoxin 6 can enhance sperm total motility and progressive motility in IVF fertilization medium.Peroxiredoxin 6 may have potential benefits for sperm preparation in assisted reproductive technology.
  • 摘要：Uncontrolled proliferation is a hallmark of cancer cells,yet the molecular mechanisms that contribute to this proliferation are unclear.Therapeutic treatment of cancer is suboptimal in many cases,with no accurate index by which to evaluate the success of treatment or patient prognosis.In this study,we explored the protein levels of nuclear phospho-eIF4E in acute myeloid leukemia(AML)cell lines and primary leukemia samples by Western blot and immunofluorescence and as well analyzed transcriptomes by RNA-seq.We found nuclear phospho-eIF4E,an exporter of oncogenic mRNAs,to be abundant in AML.Further,nuclear phospho-eIF4E abundance was significantly associated with tumor burden as well as the response of AML patients to chemotherapy.The results demonstrate“massive clustering and export of oncogenic mRNAs to the translation machinery”by highly abundant RNA-nuclear phospho-eIF4E bodies.This is an efficient mechanism that may drive the proliferation of cancer cells.Herein,nuclear phospho-eIF4E bodies were identified as potential markers of AML,which may be useful for prognosis and as targets for cancer therapy.
  • 摘要：Reviews The Dectin-1 cluster comprises seven members:CLEC-12A,CLEC-12B,CLEC-1A,CLEC-7A,CLEC-2,CLEC-9A and OLR1.These members have been demonstrated to be involved in the tumorigenesis,progression,and metastasis of several cancers.However,little is known about their roles in human lung adenocarcinoma(LUAD).The expression patterns of the Dectin-1 cluster were analyzed via the ONCOMINE and GEPIA databases.We evaluated the prognostic value of the Dectin-1 cluster in patients with LUAD using the Kaplan-Meier plotter and GEPIA.Differential expression was validated with the EMBL-EBI database,and protein expression was analyzed with the HPA database.In addition,protein-protein interaction network,GO,and KEGG analyses were conducted.Finally,the correlations between CLEC-12A and immune molecules(immune inhibitors and MHC molecules)were investigated via TISIDB and GEPIA.The expression levels of Dectin-1 cluster genes were downregulated in LUAD tissues compared to those in normal lung tissues.The expression levels of CLEC-12A,CLEC-12B,CLEC-2,and CLEC-9A correlated with tumor stage,and CLEC-12A and CLEC-12B were significantly associated with survival in patients with LUAD.The seven genes mostly participated in immune regulation processes and were involved in autoimmune disorders and hematological malignancies.Finally,correlation analyses revealed CLEC-12A expression was associated with most immune inhibitors and MHCs.CLEC-12A was positively related to PD-1,PD-L1,PD-L2,CTLA4,TIM3,and LAG3.In conclusion,our findings suggest that CLEC-12A and CLEC-12B can be used as prognostic biomarkers in LUAD.CLEC-12A expression was associated with immune checkpoint molecules,and CLEC-12A may be a potential assistant target to improve the efficacy of immune checkpoint inhibitors immunotherapy.
  • 摘要：Hypoxia affects the advancement,metastasis,and metabolism of breast cancer(BC).The circular RNA ribonuclease P RNA component H1(circRPPH1)(has_circ_0000515)is implicated in tumor progression.Nevertheless,the regulatory mechanism related to circRPPH1 in hypoxia-mediated triple-negative breast cancer(TNBC)progression is indistinct.The expression levels of circRPPH1,miR-1296-5p,tripartite motif-containing 14(TRIM14)mRNA in tissue samples and cells were examined through quantitative real-time polymerase chain reaction(qRT-PCR).Cell viability,migration,and invasion were determined with Cell Counting Kit-8(CCK-8)or transwell assays.The levels of glucose consumption and lactate production were assessed via the Glucose Assay Kit or Lactate Assay Kit.The protein levels of TRIM14,Glucose Transporter GLUT1(GLUT1),and lactic dehydrogenase A(LDHA)were detected by western blot analysis.The targeting relationship between circRPPH1 or TRIM14 and miR-1296-5p was verified with dual-luciferase reporter assay.The role of circRPPH1 was confirmed via xenograft assay.We verified that circRPPH1 and TRIM14 expression were increased while miR-1296-5p expression was decreased in BC tissues and hypoxia-cultured TNBC cells.Functionally,circRPPH1 silencing reversed the promoting effect of hypoxia on viability,migration,invasion,and glycolysis of TNBC cells.CircRPPH1 knockdown repressed decreased TNBC cell growth in vivo.Mechanistically,circRPPH1 sponged miR-1296-5p to modulate TRIM14 expression.Also,miR-1296-5p silencing restored circRPPH1 inhibition-mediated influence on the viability,migration,invasion,and glycolysis of hypoxia-treated TNBC cells.TRIM14 elevation overturned the inhibitory impact of miR-1296-5p mimic on viability,migration,invasion,and glycolysis of hypoxia-cultured TNBC cells.In conclusion,hypoxia-induced circRPPH1 fostered TNBC progression through regulation of the miR-1296-5p/TRIM14 axis,indicating that circRPPH1 was a promising target for TNBC treatment.
  • 摘要：Inorporation of etoposide(ETP)into nanoemulsion(NE)containing polyunsaturated faty adids(PUFAS)may potentially augment its antiproliferation efet on the cancer cll The current study aimed to examine the in vitro antitumor activity of a novel formulation(ETP-BC/EP-NE)produced by combining the anticancer drug(ETP)with NE(BCEP-NE)consisting of the blasck currant seed and organic ewening primrose oils.The produced formulas were physically charaterized using 2etasizer measurements.Thelr ceytotoxkc efect was testfied at concentrations ranges from 0.0001 to 5μM using CCK-8.Apoptotic and ant-invasion efects were evaluated using the assays of mitochondrtal membrane potental,annexin V-FITC double staining.DNA fragmentation,and collagen-based cell invasion.According to the zetasizer charaterization,the nano-suspensions of ETP-BC/EP-NE have z-average diameters of 87.63土3.30 nm with an average surface zeta potential of-0.605土0.003 mV.A reduction of 50%in the growth of SK-OV-3 cells was found at a distinetly lower concentration of ETP-BCEP-NE(IlCso=0.04土0.2μM)than that of ETP(ICsu=4.75土0.1μM).Resuts indicated that FTP-BCIEP-NE had a greater apoptotic ffect than FTP on SK-OV-3 cllsl which was attibuted to the larger amount of late apoptotic cells(41.9土1.05%)higher loss of mitochondrial membrane potential,and more intensive fragmented DNA The ETP-BC/EP-NE treatment suppressed the cllular invasion by 55%,whereas EIP impeded the ellular invasion by only 3%,Formulting ETP with PUFAs in NE had ameliorated the efcacy of ETP.
  • 摘要：Taro(Colocasia esculenta(L.)Schott)is an important crop in Africa,Southeast Asia,and subtropics and is used as a food and medicine.The purple color pigmentation is an appealing character in taro.We sampled taro corms of the cultivar‘Lipu Taro’at four developmental stages,including LPYS1(without purple pigment,50 days of development(DOD)),LPYS2(very few purple pigments,75 DOD),LPYS3(moderate purple pigments,115 DOD)and LPYS4(high purple pigments,205 DOD).The purpose of our study was to identify the key genes underpinning the purple pigmentation in taro based on RNA-sequencing.Through RNA-Seq,6453 differentially expressed transcripts(DETs)were identified between purple and non-purple pigmented samples.We identified 41 and 12 flavonoid and anthocyanin related DETs transcripts,respectively.These DETs were upregulated at LPYS2,LPYS3,and LPYS4 as compared to LPYS1,indicating their positive contribution to the color formation in taro.Moreover,we identified several DETs encoding for transcription factors,including MYB and bHLH,known to be major regulators of structural genes involved in the flavonoid-anthocyanin pathway.Finally,we reported several plant hormones(ethylene,auxin,gibberellin,jasmonic acid,and cytokinin)related DETs,which are predicted to play important roles in the corm coloration.Different regulation of transcripts representing the flavonoid-anthocyanin biosynthesis pathway,plant hormone transduction pathway,and transcription factors may have key roles in purple pigmentation in taro.Our findings will facilitate future research on improving the quality and appeal of taro.
  • 摘要：RPA3(Replication Protein A3)(14 kD)is a part of the canonical heterotrimeric replication protein A complex(RPA/RP-A).This study aimed to explore the functional role of RPA3 and the mechanisms of its dysregulation in breast cancer.Data from the Cancer Genome Atlas(TCGA)-breast cancer patients and GSE75688 were utilized for gene expression and survival analysis.Breast cancer cell lines MDA-MB-231 and SK-BR-3 were used for in-vitro cell studies.Clonogenic assay and immunofluorescent staining ofγ-H2AX were performed to examine radiation-induced cytotoxicity.Systemic correlation analysis was performed to identify potential transcription factors(TFs)regulating RPA3 expression.ChIP-qPCR and dual-luciferase assay were conducted to verify the transcriptional activating effect of YY1 on RPA3 expression.Bioinformatic analysis showed that RPA3 expression was upregulated in breast cancer.Its upregulation was associated with poor survival of basal-like and HER2+cases.RPA3 inhibition by siRNA reduced colony formation and increasedγ-H2AX foci formation after irradiation in MDA-MB-231 and SK-BR-3 cells.RPA3 expression was transcriptionally activated by YY1 via promoter binding in the two cell lines.Both RPA3 and YY1 expression were positively correlated with their gene-level copy numbers.RPA3 might serve as a potential target for radio-sensitization in basal-like and HER2+breast cancer.
  • 摘要：Esophageal cancer is the second most common type of cancer after lung carcinoma in the state of Jammu and Kashmir(J&K).The understanding of genetics in Esophageal cancer development is poor in the state.Genome wide association studies(GWAS)has proved to be unsurpassed tool in identification of new loci associated with different cancers.GWAS in Chinese population has identified SNP rs2294693 present in UNC5CL(UNC-5 Family C-Terminal like)to be associated with non-cardia gastric cancer.We performed a case control association study and genotyped the SNP rs2294693 using Taqman allele discrimination assay in 566 individuals(166 esophageal cancer patients and 400 controls)belonging to the J&K population.A statistically significant protective association with allelic odds ratio of 0.73(0.56–0.94 at 95%CI)and p value=0.016 was observed.This is the first study in relation to esophageal cancer in the Jammu and Kashmir population,so far it has been studied in association with gastric carcinoma in the Chinese population only.The results indicate that the polymorphism rs2294693 is associated with esophageal cancer susceptibility and the mutant(T)allele might be a protective factor for esophageal cancer among Jammu and Kashmir population.Further the functional characterization of the variation is also warranted.
  • 摘要：Overloading the intestine enterocytes with lipids induced alteration of the Golgi complex(GC;Sesorova et al.,2020)and could cause glycosylation errors.Here,using differentiated Caco-2 cells with the established 0[I]blood group phenotype(no expression of the blood antigens A and B[AgA,AgB]under normal conditions)as a model of human enterocytes we examined whether the overloading of these cells with lipids could cause errors in the Golgi-dependent glycosylation.We demonstrated that under these conditions,there were alterations of the GC and the appearance of lipid droplets in the cytoplasm.Rare cells produced AgA and AgB.This suggested that after overloading of enterocytes with lipids,AgA were mistakenly synthesized in individual enterocytes by the Golgi glycosyltransferases.These mistakes could explain why in the absence of AgA and AgB antibodies against them exist in the blood.
  • 摘要：Non-smallcell lung cancer(NSCLC)cells intake and consume glucose at high efficiency by aerobic glycolysis to maintain robust cell growth and resist cell death.MicroRNAs(miRNAs)have been known to play pivotal roles in NSCLC development partly through mediating glycolysis.However,only a few miRNAs have been experimentally confirmed as critical regulators of glycolysis in NSCLC.TCGA datasets were analyzed to screen for differentially expressed miRNAs between NSCLC and normal tissues.The function of miR-1294-5p was determined in NSCLC cells by cell proliferation,glucose uptake,lactate release,and Extracellular Acidification Rate(ECAR)assays.The target of miR-1294-5p was predicted by TargetScan and miRDB,which was further validated by flow cytometry analysis,RT-qPCR,western blotting,a dual-luciferase reporter assay,and RNA immunoprecipitation(RIP)assay.In the present study,it was found that miR-1294-5p was a significantly downregulated miRNA in lung adenocarcinoma(LUAD)and lung squamous cell carcinoma(LUSC).The overexpression of miR-1294-5p inhibited glycolysis,lactate export,ECAR,and cell proliferation in NSCLC cells.Analysis with bioinformatic tools,Western Blotting,RT-qPCR,flow cytometry analysis,dual-luciferase reporter assay,and RIP assay showed that miR-1294-5p directly bound to complementary sites in the 3’-Untranslated Region(UTR)of TMPRSS11B resulted in downregulation of TMPRSS11B expression.In addition,transfection of recombinant TMPRSS11B rescued the functions of miR-1294-5p on glycolysis and proliferation of NSCLC cells.The findings provided novel insights for understanding the regulation of glycolytic metabolism in NSCLC.
  • 摘要：Oxidative stress-mediated cell death in cardiomyocytes contributes to the development of atrial fibrillation.However,the detailed mechanisms are still unclear.In the present study,we established atrial fibrillation models in mice.The cardiomyocytes were isolated from atrial fibrillation mice and normal mice and were cultured in vitro,respectively.The results showed that cell proliferation and viability in cardiomyocytes with atrial fibrillation were significantly lower than the cells from the normal mice.Consistently,atrial fibrillation cardiomyocytes were prone to suffer from apoptotic cell death.Also,the oxidative stress and ferroptosis-associated signatures were significantly increased in atrial fibrillation cardiomyocytes compared to normal cardiomyocytes,and ferroptosis inhibitor and NAC rescued cell viability in atrial fibrillation cardiomyocytes during in vitro cell culture.In addition,low-expressed miR-143-3p was observed in atrial fibrillation cardiomyocytes compared to normal cardiomyocytes,and overexpression of miR-143-3p increased cell proliferation and inhibited cell death in atrial fibrillation cardiomyocytes.Furthermore,glutamic-oxaloacetic transaminase 1 could be negatively regulated by miR-143-3p in normal cardiomyocytes,and miR-143-3p overexpression inhibited cell ferroptosis in atrial fibrillation cardiomyocytes by sponging glutamic-oxaloacetic transaminase 1.Collectively,overexpression of miR-143-3p increased cell viability and promoted cell proliferation in cardiomyocytes with atrial fibrillation by inhibiting glutamic-oxaloacetic transaminase 1 mediated oxidative damages and cell ferroptosis.
  • 摘要：Various factors can induce cell degeneration by altering the phenotype and metabolism of cells.Mitochondria play an essential role in cellular homeostasis and function,rendering aging processes highly associated with mitochondrial function and status.Herein,we describe an aging-prone phenotype of murine skin cells caused by depletion of Rad6B(Ube2b),an E2 ubiquitin-conjugating enzyme.In this study,using Masson’s trichrome,we showed that loss of Rad6B causes physiological structure changes in mouse skin with age.In addition,a combination of western blotting experiments,transmission electron microscopy and employment of immunofluorescence staining revealed that depletion of Rad6B was characterized by an abnormal mitochondrial metabolic profile,including decreased mitochondrial biosynthesis and mitochondrial complex activities,increased ROS production and suppressed mitophagy resulting in metabolic disorders.Taken together,these results highlight an important relationship between Rad6B and skin senescence,suggesting that Rad6B plays an indispensable role in maintaining a healthy mitochondrial network and intracellular homeostasis.
  • 摘要：Apurine/pyrimidine-free endonuclease 1(APEX1)is a multifunctional enzyme that contributes to oxidization-mediated DNA-cleaved base excision repair and redox activation of transcription factors.However,the role of APEX1 during cardiomyocyte oxidative stress injury is not completely understood.In the present study,whether APEX1 protects oxidative damage-induced cardiomyocytes was investigated.mRNA and protein expression levels of APEX1 were downregulated in the mouse model of cardiac ischemia-reperfusion injury.Furthermore,the expression of APEX1 in hydrogen peroxide(H 2 O 2)-treated neonatal mice cardiomyocytes was also decreased.APEX1 knockdown aggravated H 2 O 2-treated cardiomyocyte apoptosis indexes.By contrast,APEX1 overexpression reversed H 2 O 2-induced oxidative damage,as demonstrated by decreased caspase 3 and Bax expression levels.Moreover,homeobox A5 upregulated APEX1.The results of the present study indicated that APEX1 displayed protective effects against oxidative damage,suggesting that APEX1 may serve as a unique protective strategy for cardiac ischemia-reperfusion injury.
  • 摘要：The chemokine ligand 13-chemokine receptor 5(CXCL13-CXCR5)axis has been characterized as a critical tumor-promoting signaling pathway in the tumor microenvironment(TME)in multiple types of solid tumors.In this study,we analyzed the expression profile of CXCL13 in kidney clear cell carcinoma(KIRC)and its correlation with tumor-infiltrating immune cells(TIICs).A monoclonal antibody against CXCL13 with high affinity and purity was generated in our lab for western blot and immunohistochemistry(IHC).Bioinformatic analysis was performed based on bulk-seq data from the Cancer Genome Atlas(TCGA)-KIRC and single-cell RNA-seq data from scRNASeqDB and PanglaoDB.Results showed that high CXCL13 expression in TME was associated with shorter progression-free survival(PFS),disease-specific survival(DSS),and overall survival(OS).KIRC cell lines,as well as several other cancer cell lines,had negative CXCL13 expression.IHC staining from the Human Protein Atlas(HPA)and our tissue array indicated that CXCL13 might be mainly expressed by TIICs,but not KIRC tumor cells.CXCL13 expression was strongly and positively correlated withγδT cell abundance in TME.Besides,γδT cell infiltration was associated with poor survival of KIRC.Methylation 450k array data showed that CXCL13 promoter hypomethylation was common in TIICs.The methylation level of cg16361705 within the CXCL13 promoter might play an important role in modulating CXCL13 transcription.In conclusion,our study revealed that CXCL13 expression andγδT cell infiltration in TME is associated with unfavorable survival of KIRC.TIICs,most possiblyγδT cells,are the dominant source of CXCL13 in KIRC TME.
  • 摘要：Tet methylcytosine dioxygenase 2(TET2)acts as an antioncogene that is investigated in different cancers.But the effects of TET2 in renal cell cancer(RCC)is still known little.Here,quantitative real-time PCR(qRT-PCR),Western blot,and immunofluorescence were performed to exam gene and protein expression.Cell proliferation was measured using Cell Counting Kit-8(CCK-8).Transwell assay was performed to detect cell metastasis viability.Flow cytometry was performed to analyze the cell cycle and cell apoptosis.The effects of TET2 on RCC growth in vivo was analyzed using a mouse xenograft model.We found that TET2 and miR-200c were decreased in RCC tissues,and hypermethylation of miR-200c promoter was found.Overexpression of TET2 promoted miR-200c expression by reducing miR-200c promoter methylation.Additionally,overexpression of TET2 or miR-200c suppressed cell growth and metastasis.Also,knockdown of miR-200c could moderate TET2 mediated cell growth inhibition.Furthermore,we found miR-200c directly regulates Stearoyl-CoA desaturase(SCD)gene expression.Moreover,in vivo experiment results confirmed that TET2 inhibited tumor growth.In conclusion,TET2 acts as an antioncogene in RCC by regulating the miR-200c-SCD axis and providing a potential target for RCC diagnosis and treatment.
  • 摘要：Proteintyrosine phosphatase 1B(PTP1B)inhibitionis consideredas a potentialtherapeuticfor the treatmentof cancer,type2 diabetes,andobesity.Inour presentwork,weinvestigatedtheanti-diabeticpotentialof8-hydroxydiospyrin(8-HDN)from D.lotus against the PTP1B enzyme.It showed significant inhibitory activity of PTP1B with an IC 50 value of 18.37±0.02μM.A detailed molecular docking study was carried out to analyze the binding orientation,binding energy,and mechanism of inhibition.A comparative investigation of 8-HDN in the catalytic,as well as the allosteric site of PTP1B,was performed.Binding energy data showed that compound 8-HDN is more selective for the allosteric site and hence avoids the problems associated with catalytic site inhibition.The inhibition mechanism of 8-HDN can be further investigated as an active lead compound against PTP1B by using in vitro and in vivo models.
  • 摘要：Bronchial asthma is a common chronic inflammatory disease characterized by airway hyperresponsiveness(AHR),inflammatory cell infiltration,and airway remodeling.F-box/WD repeat-containing protein 7(FBXW7),an E3 ubiquitin ligase,is required for various endothelial functions,such as cell migration,inflammation,and endothelial integrity.This study aimed to investigate the role of FBXW7 in lipopolysaccharide(LPS)-induced epithelial barrier impairment in bronchial epithelial cells in vitro.By using lentivirus-based technology,FBXW7 was overexpressed or silenced(24 h)in human bronchial epithelial(16HBE)cells,which were treated with LPS or not(24 h).Immunoprecipitation(IP)detection and Western blot analysis were used to evaluate the interaction of target proteins.Cell permeability was measured using transepithelial electrical resistance and FITC dextran flux(48 h).IL-1β,IL-18 and TNF-αin cell supernatants were measured using ELISA(48 h).The results showed that LPS stimulation suppressed FBXW7 expression in a time-and dose-dependent manner.LPS exposure decreased cell proliferation,elevated IL-1β,IL-18 and TNF-α,increased epithelial permeability,and p38 phosphorylation.These LPS-induced changes were partly compromised by FBXW7 overexpression.Similar to LPS stimulation,FBXW7 knockdown increased epithelial permeability and levels of inflammatory cytokines and p38 phosphorylation,which were,in part,blocked by apoptosis signal-regulating kinase(ASK)1 knockdown or p38 pathway inhibition.IP and Western blot analysis showed that FBXW7 interacted with ASK1.ASK1 expression was inversely associated with FBXW7 expression.FBXW7 overexpression markedly enhanced ASK1 ubiquitination.These data revealed that FBXW7 counter against inflammation and protects epithelial barrier integrity in bronchial epithelial cells by promoting ubiquitination-mediated degradation of ASK1 via the p38 pathway.
  • 摘要：Increasing evidence indicates that aberrant expressions of some microRNAs are associated with cancer progression.However,the roles and biological mechanisms of miRNA-16-5p in human non-small cell lung cancer(NSCLC)are not to be well studied.Here,we validated that the expression of miR-16-5p was decreased significantly in NSCLC samples and cell lines.The correlation between the clinicopathological features of NSCLC and the miR-16-5p expression showed that the expression of miR-16-5p in non-small cell lung cancer was linked with the advanced TNM stage,positive lymph node metastasis,with short overall survival(OS).Also,a negative correlation between miR-16-5p and Fermitin family member 2(FERMT2)was observed,implying there may be a potential link about their regulation.The hypothesis was further confirmed by in-silico analysis and dual-luciferase reporter assay.Moreover,we demonstrated that the transfections of miR-16-5p mimics could alter some biological characteristics of NSCLC cells remarkably accomplished by the expression variance of FERMT2 in vitro and in vivo assays.Summarily,this study demonstrated that miR-16-5p,as a tumor suppression factor in NSCLC by targeting FERMT2,could serve as one promising biomarker in the prediction for NSCLC patients.
  • 摘要：Chemotherapy drug resistance is the main cause leading to the relapse and metastasis of non-small cell lung cancer(NSCLC)patients.Our study aimed to investigate the mechanism of pemetrexed resistance in NSCLC.Firstly,the pemetrexed(PEM)-resistant PC-9 and A549 lung adenocarcinoma cell lines(PC-9/PEM and A549/PEM)were established.The expression of thymidylate synthase(TS)in PC-9/PEM,A549/PEM,A549,and PC-9 cells were analyzed by qRT-PCR and western blot.Then,cell viability,colony formation,migration,and invasion were performed on PEM-resistant cells transfected with TS siRNA.The role of EGFR in PEM resistance of PEM-resistant cells was investigated using EGFR siRNA.The effects of gefitinib and EGFR siRNA on EGFR/PI3K/AKT pathway and downstream signaling Cyclin D1 and E2F1 in PEM-resistant cells were analyzed.Results showed that the protein level of TS was significantly increased in A549/PEM and PC-9/PEM.TS knockdown inhibited the potency of proliferation,colony-forming potential,migration,and invasion in PEM-resistant cells.EGFR knockdown abrogated the resistance to PEM of PEM-resistant cells and suppressed the migration and invasion of PEM-resistant cells.Gefitinib treatment and EGFR knockdown respectively inhibited the EGFR/PI3K/AKT pathway and downregulated Cyclin D1 and E2F1 in PEM-resistant cells.Thus,TS might be a predictive marker for PEM resistance in NSCLC.Inhibition of the EGFR pathway abrogated the resistance to PEM and inhibited the EGFR/PI3K/AKT and downstream signaling of PEM-resistant NSCLC cell lines.
  • 摘要：Although sorafenib has been found to prolong the survival time of patients with hepatocellular carcinoma(HCC),sorafenib resistance remains an important challenge.Increasing studies have demonstrated that long noncoding RNAs(lncRNAs)contribute to drug resistance in a wide number of cancers.Human periodontal ligament stem cell(PDLSC)osteogenesis impairment-related lncRNA(POIR)is a recently defined lncRNA for which little is known regarding its function.Our study aimed to reveal the role of POIR in the development of HCC cell sorafenib resistance.The level of POIR expression in patients and tumor cells was examined by Reverse transcription-quantitative polymerase chain reaction(RT-qPCR)assay.CCK-8,EdU,and flow cytometry assay were adopted to examine cell viability,proliferation,and apoptosis,respectively.The autophagy-associated protein expressions were determined by western blotting and autophagic flux analysis.The results of this study exhibited increased POIR in HCC tissues and cells and may be correlated with sorafenib resistance.Knockdown of POIR elevated sorafenib sensitivity by suppressing autophagy in HCC cells.Mechanically,POIR knockdown upregulated miR-182-5p,implying that miR-182-5p mediates POIR regulation.MiR-182-5p overexpression significantly enhanced chemosensitivity to sorafenib,whereas miR-182-5p inhibition had the opposite effect.The sensitization of POIR siRNA to sorafenib was abolished by co-transfection with miR-182-5p inhibitor.Our findings provide a potential target for further clinical treatment of sorafenib-resistant HCC patients.
  • 摘要：Cadmium(Cd)causes oxidative stress,which leads to the oxidation of various biomolecules by the production of reactive oxygen species(ROS)to facilitate programmed cell death(PCD).The antioxidant defense system fails to detoxify ROS when it is produced in excess.Nitric oxide(NO),a gaseous free radical and a phytohormone,regulates various physiological processes of plants.Therefore,this work was undertaken to study the effects of the application of exogenous sodium nitroprusside(SNP,a NO donor)on growth parameters,oxidative stress,accumulation of secondary metabolites,and activities of antioxidant enzymes under Cd stress.Mild(50μM)and severe(200μM)Cd stress were applied to hydroponically grown pea(Pisum sativum L.)plants with or without 50μM SNP.Severe Cd stress had a substantial impact on the plants.The effectiveness of NO in reducing Cd-induced negative effects on plant height,fresh weight,dry weight,protein content,nitrite content,nitrate reductase(NR)activity,catalase activity,and peroxidase activity were investigated.Seedling development,protein content,nitrite content,nitrate reductase(NR)activity,antioxidant defense systems disruption,overproduction of reactive oxygen species,and oxidative damage were observed.The antioxidant defense system(catalase and peroxidase activities)was activated by NO,which resulted in lower lipid peroxidation and lower hydrogen peroxide(H2O2)levels in Cd-exposed plants.SNP treatment boosted endogenous NO levels and NR activity in Cd-stressed plants while also enhanced proline levels to preserve osmotic equilibrium.The presence of total phenols and flavonoids increased after SNP treatment,indicating that SNP enhanced stress recovery and boosted plant development in Cd-stressed plants.
  • 摘要：Neurodegenerative disorders are a vicious woe to the public health and wellness.Uncertainty in their underlying causes,lack of effective biomarkers for their early detection,existence of only supportive therapy,and their ever rising incidence creates an unmatched need for targeted therapies.Mesenchymal Stem Cells(MSCs)have found to be promising candidates for regenerative and remedial therapy in neurodegenerative disorders,however several biological risks and practical issues impede in their translational utility.Deriving from MSCs are certain Extracellular Vesicles(EVs),which aid in the paracrine action of MSCs and have lately gained the scientific interest for their implacability in diverse set ups.Their cargo is of utmost importance and is being explored in various different diseases like heart diseases,neuronal diseases,respiratory diseases and hepatic diseases.They thereby hold the position of a likely prospective remedial candidate for therapy against neurodegenerative disorders.
  • 摘要：Breast cancer(BC)is the most common malignant tumor and one of the top causes of cancer-related death worldwide(Sung et al.,2021).The recent advances in early tumor diagnosis coupled with more effective treatment strategies resulted in a steady increase of long-term survivors(Nardin et al.,2020;Invernizzi et al.,2022).These improved survival rates led to a significantly higher incidence of disabling complications related to breast cancer and/or its treatment(Invernizzi et al.,2020a;D’Egidio et al.,2017;Zhong et al.,2020).
  • 摘要：In this study,phosphoenolpyruvate and erythrose-4-phosphate are efficiently supplied by collaborative design of Embden-Meyerhof-Parnas(EMP)pathway and pentose phosphate(PP)pathway in Escherichia coli,thus increasing the L-tryptophan production.Firstly,the effects of disrupting EMP pathway on L-tryptophan production were studied,and the results indicated that the strain with deletion of phosphofructokinase A(i.e.,E.coli JW-5ΔpfkA)produced 23.4±2.1 g/L of L-tryptophan production.However,deletion of phosphofructokinase A and glucosephosphate isomerase is not conducive to glucose consumption and cell growth,especially deletion of glucosephosphate isomerase.Next,the carbon flux in PP pathway was enhanced by introduction of the desensitized glucose-6-phosphate dehydrogenase(zwf)and 6-phosphogluconate dehydrogenase(gnd)and thus increasing the L-tryptophan production(i.e.,26.5±3.2 g/L vs.21.7±1.3 g/L)without obviously changing the cell growth(i.e.,0.41 h^(-1) vs.0.44 h^(-1))as compared with the original strain JW-5.Finally,the effects of co-modifying EMP pathway and PP pathway on L-tryptophan production were investigated.It was found that the strain with deletion of phosphofructokinase A as well as introduction of the desensitized zwf and gnd(i.e.,E.coli JW-5 zwf243 gnd361ΔpfkA)produced 31.9±2.7 g/L of L-tryptophan,which was 47.0%higher than that of strain JW-5.In addition,the glucose consumption rate of strain JW-5 zwf243 gnd361ΔpfkA was obviously increased despite of the bad cell growth as compared with strain JW-5.The results of this study have important reference value for the following application of metabolic engineering to improve aromatic amino acids producing strains.
  • 摘要：Comparisons of gene expression profiles between primary tumors and metastasis have revealed genes that are implicated in metastasis formation.However,gene expression studies conducted on metastasis samples from the same primary site usually do not discriminate between different secondary sites.Although the change in the expression of number of genes is expected to be common to metastasis from the same primary but different secondary sites,herein the data that point to substantial differences are presented.Furthermore,the reciprocal communication between metastatic and host cells that is influencing these differences is outlined to emphasize the need for stratification of metastasis samples in gene expression studies.

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