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首页> 外文期刊>DNA and Cell Biology >Knockdown of miR-629 Inhibits Ovarian Cancer Malignant Behaviors by Targeting Testis-Specific Y-Like Protein 5
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Knockdown of miR-629 Inhibits Ovarian Cancer Malignant Behaviors by Targeting Testis-Specific Y-Like Protein 5

机译:MiR-629的敲低通过靶向睾丸特异性Y样蛋白5来抑制卵巢癌恶性行为

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摘要

Ovarian cancer (OC) is the most lethal gynecological cancer. The molecular mechanism of it is complicated, and numerous researches suggest that microRNAs are key regulators for it. This study was to investigate the pivotal role of miR-629 in the progression of OC and to reveal the possible molecular mechanism of its action. Testis-specific Y-like protein 5 (TSPYL5) is a tumor suppressor gene in various cancers, but there is little for its role in OC. OC OVCAR3 cells were transfected with the miR-629 vector, miR-629 inhibitor, and/or small interfering RNA (siRNA) targeting TSPYL5 (si-TSPYL5), respectively. After transfection, cell apoptosis, the ability of migration, and invasion were explored, as well as the level of miR-629 and TSPYL5 protein expression were detected by quantitative polymerase chain reaction and western blot. Compared with the control, there was increasing of miR-629, and decreasing of TSPYL5 and caspase 3 in OC tissue. Overexpression of miR-629 promoted the cell ability of migration and invasion and reduced OC cell apoptosis. In addition, elevated cancer inhibition ability of TSPYL5 induced by the miR-629 inhibitor was significantly blocked by inhibition of TSPYL5 (si-TSPYL5). All the above results suggested that miR-629 could promote OC proliferation, migration, and invasion by directly suppressing TSPYL5 expression, and inhibition of miR-629 might serve as a therapeutic target for OC.
机译:卵巢癌(OC)是最致命的妇科癌症。它的分子机制是复杂的,并且许多研究表明MicroRNA是它的主要调节因子。本研究是调查miR-629在oc进展中的关键作用,并揭示其作用的可能分子机制。睾丸特异性Y样蛋白5(Tspyl5)是各种癌症中的肿瘤抑制基因,但在OC中的作用几乎没有作用。将OC OVCAR3细胞用MiR-629载体,miR-629抑制剂和/或小干扰RNA(siRNA)转染靶向Tspyl5(Si-Tspyl5)。经过转染后,探索细胞凋亡,迁移能力和侵袭,以及通过定量聚合酶链反应和Western印迹检测miR-629和Tspyl5蛋白表达的水平。与对照相比,MiR-629的增加,并在OC组织中降低了Tspyl5和Caspase 3。 miR-629的过度表达促进了迁移和侵袭和减少的oc细胞凋亡的细胞能力。此外,通过抑制Tspyl5(Si-Tspyl5),MiR-629抑制剂诱导的Tspyl5的癌症抑制能力提高。所有上述结果表明,通过直接抑制Tspyl5表达,MiR-629可以促进OC增殖,迁移和侵袭,并且MiR-629的抑制可以作为OC的治疗靶标。

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