Send to

Choose Destination
J Cancer Res Ther. 2019;15(4):904-908. doi: 10.4103/jcrt.JCRT_886_18.

Up-regulation of Wnt5a inhibits proliferation and migration of hepatocellular carcinoma cells.

Author information

School of Medicine and Life Science, University of Jinan-Shandong Academy of Medical Sciences, Jinan, China.
Department of Pathology, No. 960 Hospital of People' Liberation Army, Jinan, China.
Department of Oncology, No. 960 Hospital of People' Liberation Army; Department of Cancer Immunotherapy, Shandong Cancer Hospital Affiliated to Shandong University, Jinan, China.



Increasing evidence suggests that Wnt5a plays an important role in tumorigenesis. In particular, its expression is downregulated in hepatocellular carcinoma (HCC). The aim of this study was to explore the effect of Wnt5a overexpression on HCC cells.

Materials and Methods:

We transfected the human HCC cell line SMMC-7721 with pcDNA3.1-Wnt5a overexpression vectors or empty pcDNA3.1 vectors. The expression of Wnt5a in transfected SMMC-7721 cells was confirmed by the western blot. Cell proliferation was examined by the colony formation test and cell cycle assay in vitro. The effect of Wnt5a overexpression on cell migration was studied using a scratch assay. In vivo tumorigenesis was assessed using a mouse xenograft model.


Wnt5a overexpression inhibited SMMC-7721 cell proliferation with a significant reduction in S-phase cells and an enrichment of G1-phase cells, a lower colony formation rate, and decreased tumor volumes in the xenograft model compared with those that of control tumors. The in vitro scratch assay revealed that Wnt5a overexpression diminished the capacity of cell migration, which may be mediated by the change in phosphorylated β-catenin and E-cadherin expression.


Wnt5a may act as a tumor suppressor in HCC, partly through the β-catenin/E-cadherin signaling pathway.


Hepatocellular carcinoma; SMMC-7721; Wnt5a; migration; proliferation

Free full text

Supplemental Content

Full text links

Icon for Medknow Publications and Media Pvt Ltd
Loading ...
Support Center