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微小RNA-766通过MDM4经由p53/ Bax信号通路诱导人结肠癌细胞凋亡。

miRNA-766 induces apoptosis of human colon cancer cells through the p53/Bax signaling pathway by MDM4.

作者信息

Chen Weirong, Cai Gaoyang, Liao Ziqun, Lin Kaihuang, Li Guangrong, Li Yanchong

机构信息

Department of General Surgery, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong 515041, P.R. China.

出版信息

Exp Ther Med. 2019 May;17(5):4100-4108. doi: 10.3892/etm.2019.7436. Epub 2019 Mar 26.

Abstract

miRNAs are closely associated with tumor genesis and development. The present study investigated the role of the expression of miRNA-766 in the survival of patients with colon cancer and the underlying molecular mechanisms. Reverse transcription-quantitative polymerase chain reaction analysis and microarray analysis were used to analyze the expression of miRNA-766. The results revealed that the expression of miRNA-766 was decreased in patients with colon cancer. The overall survival and disease-free survival rates of patients with colon cancer with a high expression of miRNA-766 were prolonged, compared with those with a low expression of miRNA-766. The overexpression of miRNA-766 reduced cell growth and induced apoptosis in colon cancer cells through suppression of the MDM4/p53 pathway. By contrast, the downregulation of miRNA-766 promoted cell growth and reduced apoptosis in colon cancer cells through activation of the MDM4/p53 pathway. The promotion of MDM4 attenuated the anticancer effect of miRNA-766 in colon cancer cells. These results demonstrated that miRNA-766 induced cell apoptosis in human colon cancer through MDM4/p53.

摘要

微小RNA(miRNAs)与肿瘤的发生和发展密切相关。本研究调查了miRNA - 766表达在结肠癌患者生存中的作用及其潜在的分子机制。采用逆转录定量聚合酶链反应分析和微阵列分析来检测miRNA - 766的表达。结果显示,结肠癌患者中miRNA - 766的表达降低。与miRNA - 766低表达的结肠癌患者相比,miRNA - 766高表达患者的总生存率和无病生存率延长。miRNA - 766的过表达通过抑制MDM4/p53途径减少结肠癌细胞生长并诱导其凋亡。相反,miRNA - 766的下调通过激活MDM4/p53途径促进结肠癌细胞生长并减少其凋亡。MDM4的促进作用减弱了miRNA - 766在结肠癌细胞中的抗癌作用。这些结果表明,miRNA - 766通过MDM4/p53诱导人结肠癌细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bc1/6468453/74a2feaa1be4/etm-17-05-4100-g00.jpg

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