Upregulation of MiR-1274a is Correlated with Survival Outcomes and Promotes Cell Proliferation, Migration, and Invasion of Colon Cancer.

Onco Targets Ther

Department of Gastrointestinal and Anal Disease Surgery, Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261031, People's Republic of China.

Published: July 2020

Purpose: Colon cancer has become one of the primary causes of cancer-related mortality in recent years. MicroRNAs (miRNAs) play important roles in the regulation of target genes expression. Some of these molecules are aberrantly expressed in colon cancer. The aim of this study was to investigate the potential role of miR-1274a in colon cancer.

Patients And Methods: The expression levels of miR-1274a in colon cancer tissues and cell lines were detected using RT-qPCR. The association between miR-1274a expression and clinical features was analyzed by the test. Then the Kaplan-Meier method and multivariate Cox regression analysis were used to explore the clinical prognostic significance of miR-1274a in colon cancer. Finally, the effects of miR-1274a on cell growth, migration, and invasion were investigated with the CCK-8 assay, colony formation assay, transwell migration, and invasion assays, respectively.

Results: The expression of miR-1274a was increased in colon cancer tissues and cell lines. The miR-1274a expression was associated with lymph node metastasis, vascular invasion, and TNM stage. Patients with high miR-1274a expression had a poor overall survival time compared with those with low miR-1274a expression. Upregulated miR-1274a promoted cell proliferation, migration, and invasion of colon cancer cells, while inhibition of miR-1274a suppressed these cellular activities by targeting FOXO4.

Conclusion: Our study suggested that miR-1274a might function as an oncogene in human colon cancer and be a potential prognostic biomarker and therapeutic target for the treatment of colon cancer.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373418PMC
http://dx.doi.org/10.2147/OTT.S246160DOI Listing

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