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Uc.206 通过靶向宫颈癌细胞中的 P53 来调节细胞增殖和凋亡。

Uc.206 regulates cell proliferation and apoptosis by targeting P53 in cervical cancer cells.

出版信息

Neoplasma. 2016;63(3):411-8. doi: 10.4149/310_151017N538.

DOI:10.4149/310_151017N538
PMID:26925787
Abstract

Ultraconserved regions (UCRs) are non-protein coding gene sequences with strict conserved across among different species. Emerging evidence demonstrates that UCRs encoding noncoding RNAs (ncRNAs) serve as regulators of gene expression. In recent decades, increasing evidence implicates the involvement of UCRs in carcinogenesis. Previous studies showed RNA expression of uc.206 was increased in colorectal cancer. Until now, the role of uc.206 in cervical cancers remains undefined. This study revealed that uc.206 is significantly up-regulated in cervical cancer (CC) tissue and negatively correlates with the expression of the pro-apoptotic gene P53 in RNA level. We show that uc.206 specifically targets the 3' untranslated region (3'UTR) of P53 and regulates its expression. Inhibition of uc.206 effectively delays cervical cells proliferation and promotes apoptosis, accompanied by increased expression of P53 protein. Thus, these findings suggested that uc.206 acts as a novel oncogene by targeting the P53 gene and promoting CC cell growth, which might be beneficial for cervical cancer therapy.

摘要

超保守区域(UCRs)是具有严格物种间保守性的非蛋白编码基因序列。新出现的证据表明,编码非编码 RNA(ncRNAs)的 UCRs 可作为基因表达的调节剂。在过去的几十年中,越来越多的证据表明 UCRs 参与了癌症的发生。先前的研究表明,uc.206 在结直肠癌中的 RNA 表达增加。直到现在,uc.206 在宫颈癌中的作用仍未确定。本研究表明,uc.206 在宫颈癌(CC)组织中显著上调,并在 RNA 水平上与促凋亡基因 P53 的表达呈负相关。我们表明,uc.206 特异性靶向 P53 的 3'非翻译区(3'UTR)并调节其表达。uc.206 的抑制可有效延缓宫颈细胞的增殖并促进细胞凋亡,同时 P53 蛋白的表达增加。因此,这些发现表明 uc.206 通过靶向 P53 基因并促进 CC 细胞生长而充当新型致癌基因,这可能对宫颈癌的治疗有益。

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