LncRNAs PSMG3-AS1和MEG3相互负向调控参与子宫内膜癌细胞增殖。

Shuai Huang, Jiankun Chen, Xuexiao Gao, Zhiyuan Shang, Xiao Ma, Xia Zhang, Jiayang Li, Ruoyun Yin, Xiaojing Meng
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引用次数: 1

摘要

子宫内膜癌(EC),也称为子宫癌或子宫癌,是发达国家妇女中最常诊断的生殖器癌症。我们的初步RNA-seq分析显示PSMG3-AS1和MEG3在EC组织中的表达呈负相关,表明它们之间可能存在相互作用。本研究旨在探讨两种长链非编码rna (lncRNAs) PSMG3-AS1和MEG3在EC中的相互作用。研究两种lncrna之间的相互作用在癌症生物学中是一个新的课题。采用RT-qPCR检测60例EC患者EC及配对非肿瘤组织中PSMG3-AS1和MEG3的表达。采用Pearson相关系数分析两者之间的相关性。PSMG3-AS1和MEG3在EC细胞中过表达,研究它们之间的关系。CCK-8法检测PSMG3-AS1和MEG3对EC细胞增殖的调控作用。PSMG3-AS1在EC中上调,而MEG3下调。在EC组织中,PSMG3-AS1和MEG3的表达呈负相关。在EC细胞中,PSMG3-AS1和MEG3过表达导致彼此下调。在细胞增殖实验中,PSMG3-AS1促进细胞增殖,MEG3抑制细胞增殖。此外,共转染PSMG3-AS1和MEG3表达载体的细胞的增殖率与未转染的细胞没有差异。综上所述,PSMG3-AS1和MEG3可能相互负向调控EC细胞的增殖。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LncRNAs PSMG3-AS1 and MEG3 negatively regulate each other to participate in endometrial carcinoma cell proliferation.

Endometrial carcinoma (EC), also known as corpus cancer or corpus uterine cancer, is the most frequently diagnosed genital cancer among women in developed countries. Our preliminary RNA-seq analysis revealed the inverse correlation between the expression of PSMG3-AS1 and MEG3 across EC tissues, indicating the possible interaction between them. This study aimed to explore the interaction between two long non-coding RNAs (lncRNAs) PSMG3-AS1 and MEG3 in EC. Investigation of the interaction between two lncRNAs in cancer biology is a novel topic. The expression of PSMG3-AS1 and MEG3 in EC and paired non-tumor tissues from 60 EC patients were determined by RT-qPCR. Correlations between them were analyzed by Pearson's correlation coefficient. PSMG3-AS1 and MEG3 were overexpressed in EC cells to study the relationship between them. The roles of PSMG3-AS1 and MEG3 in regulating the proliferation of EC cells were assessed by CCK-8 assay. PSMG3-AS1 was upregulated, while MEG3 was downregulated in EC. Across EC tissues, the expression of PSMG3-AS1 and MEG3 were inversely correlated. In EC cells, overexpression of PSMG3-AS1 and MEG3 resulted in the downregulation of each other. In cell proliferation assay, PSMG3-AS1 promoted cell proliferation, and MEG3 inhibited cell proliferation. Moreover, the proliferation rate of cells co-transfected with PSMG3-AS1 and MEG3 expression vectors was not different from that in cells without transfections. In conclusion, PSMG3-AS1 and MEG3 may negatively regulate each other to regulate EC cell proliferation.

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