Open AccessmiR‐709 up‐regulated in hepatocellular carcinoma, promotes proliferation and invasion by targeting GPC 5
Author(s) -
Liu Tonggang,
Zhang Xuezhong,
Sha Kaihui,
Liu Xianxian,
Zhang Liguo,
Wang Bangmao
Publication year - 2015
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12181
Subject(s) - microrna , hepatocellular carcinoma , cancer research , gentamicin protection assay , cell growth , biology , transfection , metastasis , cell culture , blot , luciferase , cell migration , cancer , gene , genetics
Objectives Hepatocellular carcinoma ( HCC ) is one of the most common cancers and is a significant leading cause of cancer‐related deaths worldwide. Emerging evidence has shown that micro RNA s (mi RNA s) are associated with cancer development and progression. However, up to now little has been known concerning the role of miR‐709 in HCC . Materials and methods Real‐time RT ‐ PCR was performed to detect expression of miR‐709 in HCC cell lines and tissues. To further understand its role in HCC , we restored its expression in HepG2 cell line through transfection with miR‐709 mimics or inhibitors. CCK ‐8 proliferation assay, migration assay and invasion assay were used to detect functional roles of miR‐709. Luciferase assay and western blotting were performed to detect the target gene of miR‐709. Results We found that miR‐709 was highly expressed in HCC tissues and in HCC cell lines by qRT ‐ PCR . Re‐expression of miR‐709 in HCC cells remarkably promoted cell migration and invasiveness in vitro . Subsequent investigation revealed that glypican‐5 ( GPC 5) was a direct and functional target of miR‐709 in HCC cells where overexpression of miR‐709 impaired GPC 5‐induced inhibition of proliferation and invasion. Finally, analysis of miR‐709 and GPC 5 levels in human HCC tissues revealed that miR‐709 inversely correlated with GPC 5 expression. Conclusions These results suggest that miR‐709 may positively regulate invasion and metastasis of HCC through targeting GPC 5.