Studies have proved the role of GAS5 in the development of different cancers. This study was undertaken to investigate the role and explore therapeutic implications of GAS5 in human cervical cancer. The results showed that GAS5 was significantly (p < 0.05) downregulated in human cervical cancer tissues. The results also showed that cervical cancer progresses with the suppression of GAS5 expression levels. Additionally, the expression of GAS5 was also significantly (p < 0.05) downregulated in human cervical cancer cell lines. Nonetheless, overexpression of GAS5 caused a remarkable decrease in the proliferation of C33A and HeLa cervical cancer cells. The decrease in the proliferation rate was attributed to the induction of apoptosis of C33A and HeLa cells which was accompanied with upregulation of Bax and suppression of Bcl-2. Additionally, GAS5 overexpression also promoted the arrest of C33A and HeLa cells at the G2/M check point of cell cycle via suppression of cyclin B1 and CDK1 expression. The transwell assays showed that GAS5 overexpression significantly (p < 0.05) inhibited the migration and invasion of the C33A and HeLa cervical cancer cells. The bioinformatics analysis as well as the dual luciferase assay showed GAS5 acts as a target of miR-135a. Interestingly, the expression of miR-135a was upregulated in the human cervical cancer cells and its suppression exerted growth inhibitory effects on the C33A and HeLa cells. However, silencing of GAS5 could nullify the effects of miR-135a suppression on the proliferation of C33A and HeLa cells. Taken together, the results of this study point towards the therapeutic implications of GAS5 in the treatment of cervical cancer.

中文翻译：

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长的非编码RNA GAS5通过诱导凋亡和细胞周期停滞来调节人宫颈癌细胞的生长和转移。

研究证明了GAS5在不同癌症的发展中的作用。进行这项研究以调查GAS5在人宫颈癌中的作用并探讨其治疗意义。结果表明，GAS5在人宫颈癌组织中显着下调（p <0.05）。结果还表明宫颈癌随着GAS5表达水平的抑制而发展。另外，GAS5的表达在人宫颈癌细胞系中也显着下调（p <0.05）。尽管如此，GAS5的过度表达导致C33A和HeLa宫颈癌细胞的增殖显着下降。增殖速率的降低归因于诱导C33A和HeLa细胞凋亡，并伴随Bax的上调和Bcl-2的抑制。另外，GAS5的过表达还通过抑制细胞周期蛋白B1和CDK1的表达，促进了C33A和HeLa细胞在细胞周期的G2 / M检查点停滞。Transwell分析表明，GAS5过表达显着（p <0.05）抑制了C33A和HeLa宫颈癌细胞的迁移和侵袭。生物信息学分析以及双重荧光素酶测定表明GAS5充当miR-135a的靶标。有趣的是，miR-135a的表达在人宫颈癌细胞中被上调，其抑制作用对C33A和HeLa细胞产生了生长抑制作用。然而，GAS5沉默可能会使miR-135a抑制作用对C33A和HeLa细胞增殖的影响无效。两者合计，这项研究的结果指向GAS5在宫颈癌治疗中的治疗意义。