Open AccessLentiviral‐mediated microRNA‐26b up‐regulation inhibits proliferation and migration of hepatocellular carcinoma cells
Author(s) -
Lin ChunZhong,
Ou RongWen,
Hu YuHai
Publication year - 2018
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1016/j.kjms.2018.05.003
Subject(s) - microrna , cancer research , transfection , metastasis , hepatocellular carcinoma , western blot , cell growth , cell culture , mtt assay , medicine , biology , oncology , cancer , gene , genetics
Hepatocellular carcinoma (HCC) is a frequently occurred malignancy worldwide with a high mortality. The treatment for HCC is still controversial. Emerging evidences have demonstrated that microRNAs (miRs) play a role in HCC. This study aims to investigate the effects of lentiviral‐mediated miRNA‐26b (miR‐26b) on the proliferation and metastasis of HCC cells. The normal hepatic cell line HL‐7702 and HCC cell lines HepG2 (without metastatic potential), SMMC‐7721 (with low metastatic potential) and MHCC97H (with high metastatic potential) were purchased for our experiment. The lentiviral‐mediated miR‐26b overexpression (miR‐26b‐LV) and low expression (sh‐miR‐26b) were constructed to transfect the cells. The miR‐26b expression and expressions of Karyopherin α‐2 (KPNA2), matrix metalloproteinase 1 (MMP‐1), MMP‐7 and MMP‐14 were determined by RT‐qPCR and western blot analysis. The proliferation and metastasis of transfected HCC cells were detected by MTT and Transwell assay respectively. The miR‐26b expressions were decreased significantly in MHCC97H cells. With lentiviral‐mediated miR‐26b overexpression, the proliferation and migration of HepG2, MHCC97H and SMMC‐7721 cells were decreased significantly. The RT‐qPCR and western blot analysis results revealed that the mRNA and protein expressions of KPNA2, MMP‐1, MMP‐7 and MMP‐14 were decreased by lentiviral‐mediated miR‐26b overexpression. All the above indexes in the HepG2, MHCC97H and SMMC‐7721 cells treated by sh‐miR‐26b exhibited opposite trends. These results show that overexpressed miR‐26b could inhibit the proliferation and metastasis of HCC cells significantly, which provides a novel target and theoretical foundation for the treatment of HCC.