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Long Noncoding RNA PVT1 Promotes Melanoma Progression via Endogenous Sponging miR-26b

机译:长的非致RNA PVT1通过内源海绵MIR-26B促进黑色素瘤进展

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摘要

Melanoma is an extremely aggressive malignant skin tumor with a high mortality. Various long noncoding RNAs (IncRNAs) have been reported to be associated with the oncogenesis of melanoma. The purposes of this study were to investigate the potential role of IncRNA PVT1 in melanoma progression and to explore its possible mechanisms. A total of 35 patients who were diagnosed with malignant melanoma were enrolled in this study. Expression of PVT1 was significantly upregulated in melanoma tissue and was associated with a poor prognosis. Loss-of-function experiments showed that PVT1 knockdown markedly suppressed the proliferation activity, induced cell cycle arrest at the G(0)/G(1) phase, and enhanced the apoptosis of melanoma cell lines. Bioinformatics analysis and dual-luciferase reporter assay revealed that PVT1 directly bound to miR-26b, which had been verified to be a tumor suppressor in melanoma. Moreover, further functional rescue experiments revealed that PVT1 knockdown could observably reverse the tumor-promoting role of the miR-26b inhibitor. Overall, our study demonstrates the oncogenic role of PVT1 as a miR-26b sponge, possibly providing a novel therapeutic target for melanoma.
机译:黑色素瘤是一种极具侵袭性的恶性皮肤肿瘤,具有高死亡率。据报道,据报道,各种长的非划分的RNA(Incrnas)与黑素瘤的血管瘤的血管生成相关。该研究的目的是探讨IncRNA PVT1在黑素瘤进展中的潜在作用,并探讨其可能的机制。共有35例被诊断患有恶性黑素瘤的患者。黑色素瘤组织中PVT1的表达显着上调,预后不良。功能丧失实验表明,PVT1敲低明显抑制了增殖活性,在G(0)/ g(1)相时诱导细胞周期停滞,增强了黑素瘤细胞系的凋亡。生物信息学分析和双荧光素酶报告器测定显示PVT1直接与miR-26b结合,已被验证是黑色素瘤中的肿瘤抑制因素。此外,进一步的功能救援实验表明,PVT1敲低可以观察逆转MiR-26B抑制剂的肿瘤促进作用。总体而言,我们的研究证明了PVT1作为MiR-26B海绵的致癌作用,可能为黑色素瘤提供新的治疗靶标。

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