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Long Noncoding RNA Urothelial Carcinoma-Associated 1 Promotes the Proliferation and Metastasis of Human Lung Tumor Cells by Regulating MicroRNA-144

机译:长度非编码RNA尿路上皮癌相关1通过调节MicroRNA-144来促进人肺肿瘤细胞的增殖和转移

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Long non-coding RNA urothelial carcinoma associated 1 (lncRNA UCA1) has gained more attention in recent years due to its oncogenic roles in various cancers. MicroRNA-144 (miR-144) participates in the regulation of many cancer cells growth. This study investigated the interaction between lncRNA UCA1 and miR-144 in lung cancer cells. The potential downstream protein of miR-144 was also assessed. Our results found that lncRNA UCA1 was highly expressed in human lung cancer A549, H517, H4006, H1299 and H1650 cells compared to normal embryonic lung WI-38 and HEL-1 cells. Knockdown of lncRNA UCA1 significantly inhibited lung cancer A549 cell viability, migration, invasion and cell cycle progression, but promoted cell apoptosis. Besides, we found that lncRNA UCA1 was bound to miR-144. miR-144 participated in the regulation effects of lncRNA UCA1 on A549 cell viability, migrataion, invasion, cell cycle transition and cell apoptosis. In addition Pre-B cell leukemia homeobox 3 (PBX3) was found to be a direct target gene of miR-144. Overexpression of PBX3 promoted A549 cell proliferation and metastasis. Suppression of PBX3 had an opposite effects.
机译:由于各种癌症的致癌作用,近年来,近年来,长期非编码RNA尿路上皮癌患者近年来越来越关注。 MicroRNA-144(MIR-144)参与许多癌细胞生长的调节。本研究研究了LNCRNA UCA1和MIR-144在肺癌细胞中的相互作用。还评估了miR-144的潜在下游蛋白。我们的结果发现,与常规胚胎肺Wi-38和HEL-1细胞相比,LNCRNA UCA1在人肺癌A549,H517,H4006,H1299和H1650细胞中高度表达。 LNCRNA UCA1的敲低显着抑制肺癌A549细胞活力,迁移,侵袭和细胞周期进展,但促进细胞凋亡。此外,我们发现LNCRNA UCA1与miR-144结合。 MIR-144参与了LNCRNA UCA1对A549细胞活力,迁移,侵袭,细胞周期转换和细胞凋亡的调节作用。此外,发现Be-B细胞白血病Homeobox 3(PBX3)是miR-144的直接靶基因。 PBX3的过度表达促进了A549细胞增殖和转移。 PBX3的抑制具有相反的效果。

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