Blockade of miR-3614 maturation by IGF2BP3 increases TRIM25 expression and promotes breast cancer cell proliferation

EBioMedicine
Zhenzhen WangChen Huang

Abstract

The cross-talk between RNA binding proteins (RBPs) and microRNAs (miRNAs) in the regulation of gene expression is a complex process. Here, we describe a new mode of regulation of TRIM25 expression mediated by an antagonistic interplay between IGF2BP3 and miR-3614-3p. The expression level of TRIM25, IGF2BP3, pri-miR-3614 and miR-3614-3p in breast cancer (BC) tissues, non-tumor tissues and BC cell lines were detected by qRT-PCR, Western blot and Immunohistochemistry (IHC). Binding of miR-3614-3p and IGF2BP3 to TRIM25 RNA was verified using luciferase activation assays, RNA immunoprecipitation (RIP) and biotin pull-down assays. In vitro and in vivo loss- and gain-of-function studies were performed to reveal the effects and related mechanism of IGF2BP3-miR-3614-3p-TRIM25 axis in in breast cancer cells proliferation. We found that an intragenic miRNA-3614-3p inhibits the expression of its host gene TRIM25 by binding to its 3'- untranslated region (UTR). Interestingly, IGF2BP3 can competitively occupy this binding site and inhibit miRNA-3614 maturation, thereby protecting TRIM25 mRNA from miR-3614-mediated degradation. The overexpression of miR-3614-3p dramatically inhibited breast cancer cell growth through the downregulation of TRI...Continue Reading

Citations

May 6, 2019·International Journal of Molecular Sciences·Xiaoyong PanYu-Dong Cai
Sep 13, 2019·Cellular & Molecular Immunology·Akhilesh Kumar, Himanshu Kumar
Jul 17, 2020·Non-coding RNA·Jun Sheng Wong, Yoke Kqueen Cheah
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Feb 6, 2020·Frontiers in Cell and Developmental Biology·Caterina Mancarella, Katia Scotlandi
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Methods Mentioned

BETA
transfection
Assay
immunoprecipitation
RIP
Pull-Down
fluorescence activated cell sorting
antisense oligonucleotides
flow
xenograft
xenografts

Software Mentioned

TargetScan
RegRNA
SPSS
CellQuest

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