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miR-141 promotes colon cancer cell proliferation by inhibiting MAP2K4

MicroRNAs (miRNAs or miRs) can function as tumor-suppressor or oncogenic genes. Upregulation of miRNA-141 has been frequently observed in colorectal cancer (CRC) samples. The experimentally observed targets of miR-141 include the tumor-suppressor gene mitogen-activated protein kinase kinase 4 (MAP2K...

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Detalles Bibliográficos
Autores principales: Ding, Lei, Yu, Li-Li, Han, Ning, Zhang, Bu-Tian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403415/
https://www.ncbi.nlm.nih.gov/pubmed/28454307
http://dx.doi.org/10.3892/ol.2017.5653
Descripción
Sumario:MicroRNAs (miRNAs or miRs) can function as tumor-suppressor or oncogenic genes. Upregulation of miRNA-141 has been frequently observed in colorectal cancer (CRC) samples. The experimentally observed targets of miR-141 include the tumor-suppressor gene mitogen-activated protein kinase kinase 4 (MAP2K4). The aim of the present study was to investigate the role of miR-141 in the proliferation of colonic cancer. Western blotting, immunohistochemistry and reverse transcription-quantitative polymerase chain reaction were used to detect the expression levels of miR-141 and MAP2K4 in colonic adenocarcinoma (CAC) and adjacent non-cancerous (NC) tissue samples, as well as in human CAC cell lines (HT29, T94 and LS174). MTT assay was used to investigate the proliferation and apoptosis of these three cell lines. The expression levels of miR-141 were significantly upregulated in clinical samples of CAC, compared with adjacent NC tissues. By contrast, MAP2K4 was downregulated in CAC. The in vitro assays demonstrated that overexpression of miR-141 resulted in cell proliferation of CAC by inhibiting MAP2K4 activity. Our study suggests that targeting the miR-141-MAP2K4 signaling pathway may represent a novel approach for the treatment of CRC.