In this study, we investigated how miR-10b-3p regulated the proliferation, migration, invasion in hepatocellular carcinoma (HCC) at both invitro and invivo levels. CMTM5 was among the differentially expressed genes (data from TCGA). The expression of miR-10b-3p and CMTM5 was detected by qRT-PCR and Western blot (WB). TargetScan was used to acquire the binding sites. Dual-luciferase reporter gene assay was used to verify the direct target relationship between miR-10b-3p and CMTM5. WB analysis proved that miR-10b-3p suppressed CMTM5 expression. Furthermore, proliferation, invasion and migration of HCC cells were measured by MTT assay, colony formation assay, transwell assay and wound-healing assay, respectively. Kaplan-Meier plotter valued the overall survival of CMTM5. Finally, xenograft assay was also conducted to verify the effects of miR-10b-3p/CMTM5 axis invivo. Up-regulation of miR-10b-3p and down-regulation of CMTM5 were detected in HCC tissues and cell lines. CMTM5 was verified as a target gene of miR-10b-3p. The overexpression of CMTM5 contributed to the suppression of the proliferative, migratory and invasive abilities of HCC cells. Moreover, the up-regulation of miR-10b-3p and down-regulation of CMTM5 were observed to be associated with worse overall survival. Lastly, we have confirmed the carcinogenesis-related roles of miR-10b-3p and CMTM5 invivo. We concluded that the up-regulation of miR-10b-3p promoted the progression of HCC cells via targeting CMTM5.
[1]Jilin Univ, Dept Hepatobiliary & Pancreas Surg, China Japan Union Hosp, Changchun, Jilin, Peoples R China.
[2]Changchun Med Coll, Teachers Off Clin & Med Nursing, Changchun, Jilin, Peoples R China.
(8.0+极速模式)