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microRNA-200b and microRNA-200c promote colorectal cancer cell proliferation via targeting the reversion-inducing cysteine-rich protein with Kazal motifs
Journal article   Open access   Peer reviewed

microRNA-200b and microRNA-200c promote colorectal cancer cell proliferation via targeting the reversion-inducing cysteine-rich protein with Kazal motifs

Yi Pan, Hongwei Liang, Weixu Chen, Hongjie Zhang, Nan Wang, Feng Wang, Suyang Zhang, Yanqing Liu, Chihao Zhao, Xin Yan, …
RNA biology, v 12(3), pp 276-289
01 Mar 2015
PMID: 25826661
url
https://www.tandfonline.com/doi/pdf/10.1080/15476286.2015.1017208?needAccess=trueView
Published, Version of Record (VoR) Open
url
https://doi.org/10.1080/15476286.2015.1017208View
Published, Version of Record (VoR) Open

Abstract

Biochemistry & Molecular Biology Life Sciences & Biomedicine Science & Technology
MicroRNA-200b and microRNA-200c (miR-200b/c) are 2 of the most frequently upregulated oncomiRs in colorectal cancer cells. The role of miR-200b/c during colorectal tumorigenesis, however, remains unclear. In the present study, we report that miR-200b/c can promote colorectal cancer cell proliferation via targeting the reversion-inducing cysteine-rich protein with Kazal motifs (RECK). Firstly, bioinformatics analysis predicted RECK as a conserved target of miR-200b/c. By overexpressing or knocking down miR-200b/c in colorectal cancer cells, we experimentally validated that miR200b/c are direct regulators of RECK. Secondly, an inverse correlation between the levels of miR-200b/c and RECK protein was found in human colorectal cancer tissues and cell lines. Thirdly, we demonstrated that repression of RECK by miR-200b/c consequently triggered SKP2 (S-phase kinase-associated protein 2) elevation and p27(Kip1) (also known as cyclin-dependent kinase inhibitor 1B) degradation in colorectal cancer cells, which eventually promotes cancer cell proliferation. Finally, promoting tumor cell growth by miR-200b/c-targeting RECK was also observed in the xenograft mouse model. Taken together, our results demonstrate that miR-200b/c play a critical role in promoting colorectal tumorigenesis through inhibiting RECK expression and subsequently triggering SKP2 elevation and p27(Kip1) degradation.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
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