MiR-128-1-5p inhibits cell proliferation and induces cell apoptosis via targeting PRKCQ in  colorectal cancer

Abstract

Background MicroRNAs (miRNAs) are a type of highly conserved and endogenous noncoding RNA which can regulate various cellular processes, including cell proliferation, differentiation, apoptosis, migration and metastasis. Aberrant expression of miR-128-5p, has been shown to be a key regulator in tumorigenesis and cancer development. But the role and the underlying molecular mechanisms of miR-128 in CRC still remain largely unknown. Methods The expression and clinical significances of miR-128-1-5p in colorectal cancer tissues and cell lines was quantified by qRT-PCR. Stably transfected cell lines were established by infecting SW620 and LOVO cells with lentiviruses. The functions of miR-128-1-5p were measured by CCK-8 assay, Annexin V- DY-634 PI Apoptosis Staining / Detection, and Xenograft model. Western blotting, immunohistochemistry (IHC), luciferase reporter assays and Bioinformatic Analysis were also used in this study. Results MiR-128-1-5p was downregulated in CRC and was associated with optimal survival in CRC. Overexpression of miR-128-1-5p inhibited cell proliferation and induced cell apoptosis. Protein tyrosine kinase C theta isoform (PRKCQ) was a direct target of miR-128-1-5p and was involved in miR-128-1-5p-mediated proliferation and apoptosis. Conclusions These results provide novel insight into the role of miR-128-1-5p in CRC. Overexpression of miR-128-1-5p was associated with cell proliferation and apoptosis in CRC. Knockdown of miR-128-1-5p reduced CRC growth by modulating PRKCQ expression and is a possible new therapeutic target for patients with CRC.