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miR‐148‐3p and miR‐152‐3p synergistically regulate prostate cancer progression via repressing KLF4
Author(s) -
Feng Feng,
Liu Hui,
Chen Aiping,
Xia Qinghua,
Zhao Yong,
Jin Xunbo,
Huang Jianjun
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28984
Subject(s) - klf4 , in vivo , prostate cancer , microrna , cancer research , downregulation and upregulation , untranslated region , luciferase , in vitro , cell growth , cancer , biology , chemistry , cell culture , transcription factor , messenger rna , transfection , biochemistry , gene , sox2 , genetics
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.