miR-148-3p and miR-152-3p synergistically regulate prostate cancer progression via repressing KLF4

被引:54
|
作者
Feng, Feng [1 ,2 ]
Liu, Hui [1 ]
Chen, Aiping [3 ]
Xia, Qinghua [1 ]
Zhao, Yong [1 ]
Jin, Xunbo [1 ]
Huang, Jianjun [4 ]
机构
[1] Shandong Univ, Shandong Prov Hosp, Dept Urol, Jinan, Shandong, Peoples R China
[2] Shandong Univ, Sch Med, Jinan, Shandong, Peoples R China
[3] Liaocheng Peoples Hosp, 67 Western Dongchang Rd, Liaocheng 252000, Shandong, Peoples R China
[4] Acad Mil Med Sci, Lab Tumor & Mol Biol, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
apoptosis; Kruppel-like factor 4; miR-148-3p; miR-152-3p; prostate cancer; CELL-PROLIFERATION; HEPATOCELLULAR-CARCINOMA; PROGNOSTIC VALUE; STEM-CELLS; MICRORNA-148A; EXPRESSION; INVASION; FAMILY; GENE; STATISTICS;
D O I
10.1002/jcb.28984
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background miR-148-3p and miR-152-3p as the tumor suppressors have been reported in various cancer types. Our study is aimed to discuss the synergistic effect of miR-148-3p and miR-152-3p in prostate cancer (PCa). Methods Bioinformatics algorithm and luciferase reporter assays were used to verify whether miR-148-3p and 152-3p could bind with the 3 '-untranslated region (3 '-UTR) of Kruppel-like factor 4 (KLF4). PCa cell growth in vivo was analyzed using the mouse xenograft tumor model. Results miR-148-3p and miR-152-3p were reduced in PCa tumor tissues. Moreover, the protein expression of KLF4 was increased in PCa tissues. The 3 '-UTR of KLF4 contained the conserved binding sites with miR-148-3p and miR-152-3p. The mimics or inhibitors of miR-148-3p and/or miR-152-3p could downregulated or upregulated KLF4 expression, respectively. miR-148-3p and miR-152-3p-induced PCa cell growth inhibition were observed both in vivo and in vitro. KLF4 overexpression had the ability to neutralize the antitumor effect of miR-148-3p/152-3p in vivo and in vitro. Conclusion miR-148-3p/152-3p family could serve as tumor suppressors in PCa via repressing KLF4.
引用
收藏
页码:17228 / 17239
页数:12
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