MicroRNA-149 Suppresses Colorectal Cancer Cell Migration and Invasion by Directly Targeting Forkhead Box Transcription Factor FOXM1

Background/Aims: The aim of this study is to investigate the clinicopathological and prognostic values of miR-149 expression and its roles in colorectal cancer (CRC) progression. Methods: qRT-PCR was performed to detect miR-149 expression in CRC cell lines or tissues. Also, the clinical significance...

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Published inCellular physiology and biochemistry Vol. 35; no. 2; pp. 499 - 515
Main Authors Xu, Kai, Liu, Xiaobei, Mao, Xiaobei, Xue, Lijun, Wang, Rui, Chen, Longbang, Chu, Xiaoyuan
Format Journal Article
LanguageEnglish
Published Basel, Switzerland Cell Physiol Biochem Press GmbH & Co KG 01.01.2015
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Summary:Background/Aims: The aim of this study is to investigate the clinicopathological and prognostic values of miR-149 expression and its roles in colorectal cancer (CRC) progression. Methods: qRT-PCR was performed to detect miR-149 expression in CRC cell lines or tissues. Also, the clinical significance of miR-149 expression was investigated. The study further explored whether miR-149 inhibits migration and invasion of CRC cells by targeting the mammalian Forkhead Box M1 (FOXM1). Results: miR-149 was significantly downregulated in CRC tissues, and low miR-149 expression was observed to be significantly correlated with lymph node or distant metastasis and advanced TNM stage of CRC patients. Patients with low miR-149 expression showed poorer prognosis than those with high miR-149 expression, and multivariate analyses indicated that status of miR-149 expression might be an independent prognostic factor. Gain- and loss - of - function assays indicated that miR-149 significantly inhibited growth, migration and invasion of CRC cells by targeting FOXM1. Furthermore, FOXM1 was significantly uiregulated in CRC tissues and inversely correlated with miR-149 expression. Conclusions: mR-149 was an independent prognostic factor and could inhibit migration and invasion of CRC cells, at least partially by targeting FOXM1.
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ISSN:1015-8987
1421-9778
DOI:10.1159/000369715