MicroRNA-378-5p Suppresses Cell Proliferation And Induces Apoptosis In Colorectal Cancer Cells By Targeting BRAF

Background: Colorectal cancer possesses the third highest incidence of human malignant diseases that account for approximately 9.4% of worldwide cancer cases. According to the International Agency for Research on Cancer, about 1 million new cases were detected each year. Much effort has been made on the study of the biological mechanism of CRC and a large number of tumor suppressor genes and oncogenes have been reported recent years. However, the molecular mechanisms underlying the development of CRC are still poorly understood. microRNAs(miRNAs) are a group of small non-coding RNAs play important roles in gene translation. Dysregulation of miR-378-5p have been reported in numerous human cancers including colorectal cancer(CRC). However, its role in CRC carcinogenesis remains poorly defined. The purpose of this study was to figure out the role of miR-378-5p in CRC pathogenesis.Methods: Quantitative reverse transcription polymerase chain reaction(q RT-PCR) was designed to investigate the expression pattern of miR-378-5p in CRC tissues and cell lines. CCK8 assay, cell cycle analysis and apoptosis detection were performed to detect the effect of miR-378-5p overexpression on the biological functions of CRC cells. Luciferase reporter assay was conducted to validate the putative target of miR-378-5p. The effect of miR-378-5p on endogenous level of putative target was verified by q RT-PCR and western blot.Results: Level of miR-378-5p was greatly decreased in CRC tissues compared with adjacent normal tissues and in CRC cells. Overexpression of miR-378-5p suppressed the proliferation of CRC cells by arresting the cells in G0/G1 phase and could induce apoptosis in CRC cells. BRAF was a direct target of miR-378-5p and the levels of BRAF mRNA and protein were greatly decreased by overexpression of miR-378-5p.Conclusions: miR-378-5p may act as a tumor suppressor in CRC. The decreased proliferation of CRC cells through overexpression of miR-378-5p suggests it may be a potential therapeutic target of CRC.