首页> 外文期刊>Neoplasma: Journal of Experimental and Clinical Oncology >Long non-coding RNA MEG3 inhibits the proliferation of cervical carcinoma cells through the induction of cell cycle arrest and apoptosis.
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Long non-coding RNA MEG3 inhibits the proliferation of cervical carcinoma cells through the induction of cell cycle arrest and apoptosis.

机译:长非编码RNA MEG3通过诱导细胞周期停滞和凋亡来抑制子宫颈癌细胞的增殖。

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摘要

Cervical cancer remains an important public health problem worldwide. New and effective therapeutic strategies targeting cervical cancer are urgently needed. Long non-coding RNAs (lncRNAs) are newly identified regulators in tumorigenesis and tumor progression. To investigate the role of lncRNA MEG3 in the development of cervical cancer, we examined MEG3 expression in 18 pairs of cervical cancer and matched adjacent non-neoplastic tissues. Real-time quantitative RT-PCR (qRT-PCR) results showed high expression levels of MEG3 in non-neoplastic tissues, but markedly lower levels in cancer tissues. We further investigated whether the restoration of MEG3 expression might affect the proliferation of cervical carcinoma cells. Ectopic expression of MEG3 inhibited the proliferation of human cervical carcinoma cells HeLa and C-33A in vitro. On the other hand, knockdown of MEG3 promoted the growth of well-differentiated cervical carcinoma HCC94 cells. Further investigation into the mechanisms responsible for the growth inhibitory effects revealed that overexpression of MEG3 resulted in the induction of G2/M cell cycle arrest and apoptosis. These results identified an important role of MEG3 in the molecular etiology of cervical cancer and implicated the potential application of MEG3 in cervical cancer therapy.
机译:宫颈癌仍然是世界范围内重要的公共卫生问题。迫切需要针对宫颈癌的新的有效治疗策略。长的非编码RNA(lncRNA)是新近确定的肿瘤发生和肿瘤进展的调节剂。为了研究lncRNA MEG3在子宫颈癌发展中的作用,我们检查了MEG3在18对子宫颈癌和匹配的非肿瘤组织中的表达。实时定量RT-PCR(qRT-PCR)结果显示,MEG3在非肿瘤组织中的表达水平很高,但在癌组织中的表达水平则明显较低。我们进一步研究了MEG3表达的恢复是否可能影响宫颈癌细胞的增殖。 MEG3的异位表达在体外抑制人宫颈癌细胞HeLa和C-33A的增殖。另一方面,敲低MEG3促进分化良好的宫颈癌HCC94细胞的生长。对负责生长抑制作用的机制的进一步研究表明,MEG3的过表达导致G2 / M细胞周期停滞和凋亡的诱导。这些结果确定了MEG3在宫颈癌的分子病因学中的重要作用,并暗示了MEG3在宫颈癌治疗中的潜在应用。

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