文献类型：期刊文献

英文题名：MiR-27a-3p functions as an oncogene in gastric cancer by targeting BTG2

作者：Zhou, Lin[1];Liang, Xin[2,3];Zhang, Lingling[2,3];Yang, Liyan[2,3];Nagao, Norio[4];Wu, Hongkun[1];Liu, Chang[1];Lin, Shengchao[2,3];Cai, Guoxiang[5];Liu, Jianwen[2,3]

机构：[1]Second Mil Med Univ, Changzhen Hosp, Dept Lab Med, Shanghai 200003, Peoples R China;[2]East China Univ Sci & Technol, Sch Pharm, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[3]East China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab New Drug Design, Shanghai 200237, Peoples R China;[4]Prefectural Univ Hiroshima, Dept Life & Environm Sci, Shobara 7270023, Japan;[5]Fudan Univ, Shanghai Canc Ctr, Dept Colorectal Surg, Shanghai 200032, Peoples R China

年份：2016

卷号：7

期号：32

起止页码：51943

外文期刊名：ONCOTARGET

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000385429100093)】；

基金：This work was supported by Shanghai Committee of Science and Technology (No. 13140902300), Nano Science and Technology Special Funding of Shanghai Committee of Science and Technology (No. 11nm0503700), the Shanghai Committee of Science and Technology grant (11DZ2260600) and Pujiang Shanghai Talent Project (15PJD004).

语种：英文

外文关键词：miR-27a-3p; apoptosis; BTG2; gastric cancer; cell proliferation

摘要：microRNA-27a (miR-27a) is frequently dysregulated in human carcinoma, including gastric cancer. The B-cell translocation gene 2 (BTG2) has been implicated in gastric carcinogenesis. However, till now, the link between miR-27a and BTG2 in gastric cancer has not been reported. Here, we found that two isoforms of mature miR-27a, miR-27a-5p and miR-27-3p, were both frequently overexpressed in gastric cancer tissues and cell lines, whereas the expression level of miR-27-3p in gastric cancer was significantly higher than that of miR-27a-5p. And overexpression of miR27a-3p, but not miR-27a-5p, markedly promoted gastric cancer cell proliferation in vitro as well as tumor growth in vivo. Further experiments revealed that BTG2 was a direct and functional target of miR-27a-3p in gastric cancer and miR-27a-3p inhibition obviously up-regulated the expression of BTG2. In turn, overexpression of BTG2 triggered G1/S cell cycle arrest, induced subsequent apoptosis, and inhibited C-myc activation following Ras/MEK/ERK signaling pathway, which involved in the biological effects of miR-27a-3p/BTG2 axis on gastric carcinogenesis and cancer progression. Overall, these results suggested that the miR-27a-3p/BTG2 axis might represent a promising diagnostic biomarker for gastric cancer patients and could be a potential therapeutic target in the management of gastric cancer.