Long noncoding RNA UCID sponges miR‑152‑3p to promote colorectal cancer cell migration and invasion via the Wnt/β‑catenin signaling pathway
Author(s) -
Libin Sun,
Shufen Zhao,
Jingjuan Zhu,
Xiangan Han,
TiDong Shan
Publication year - 2020
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2020.7670
Subject(s) - wnt signaling pathway , biology , competing endogenous rna , microrna , long non coding rna , gene knockdown , oncogene , cancer research , downregulation and upregulation , cell cycle , colorectal cancer , cyclin dependent kinase 6 , microbiology and biotechnology , cell , cancer , signal transduction , genetics , gene , cyclin d1
Research has shown that long noncoding RNAs (lncRNAs) play significant roles in colorectal cancer (CRC). However, the role of lnc‑UCID (lncRNA upregulating CDK6 by interacting with DHX9) in CRC remains largely unknown. In the present study, analyses revealed that lnc‑UCID was markedly upregulated in CRC compared with that in normal specimens. Functional experiments showed that the depletion of lnc‑UCID inhibited CRC cell invasion and migration significantly, while overexpression of lnc‑UCID had the opposite effect. A candidate target of lnc‑UCID, microRNA miR‑152‑3p, was identified using bioinformatic analysis. Moreover, in CRC tissue, we noted an inverse correlation between miR‑152‑3p and lnc‑UCID expression levels. Overexpression and knockdown experiments revealed opposing roles for miR‑152‑3p and lnc‑UCID, suggesting that lnc‑UCID negatively regulates miR‑152‑3p. Luciferase reporter assays demonstrated that miR‑152‑3p directly targets lnc‑UCID. The results suggest that lnc‑UCID acts as an endogenous miRNA sponge, competing for miR‑152‑3p binding and thereby regulating the miRNA's targets. Overall, we propose that the lnc‑UCID/miR‑152‑3p/Wnt/β‑catenin signaling axis represents a novel mechanism that explains the migration and invasion of CRC.
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