Research Paper Volume 13, Issue 17 pp 21216—21231

Dual roles of WISP2 in the progression of hepatocellular carcinoma: implications of the fibroblast infiltration into the tumor microenvironment

Upregulation of WISP2 in HCC is related to inhibition of the malignant phenotype in vitro, while no difference in proliferation was found in subcutaneous tumorigenesis in vivo. (A) The expression of WISP2 was diverse in different tumour cell lines in the CCLE database. (B) The expression of WISP2 in 76% HCC cell lines, including Hep3B and HepG2, were low in CCLE database. (C) The expression of WISP2 was determined in Hep3B and HepG2, and confirmed using immunoblotting and immunocytochemistry. (D) Overexpression of WISP2 significantly inhibited the migration and invasiveness in Hep3B and HepG2 HCC cells. (E) Proliferation in Hep3B and HepG2 HCC cells that overexpress WISP2 or control cells was examined using a plate colony formation assay, and overexpression of WISP2 significantly impaired the colony formation. (F) Proliferation was assessed using a CCK8 assay, and overexpression of WISP2 significantly inhibited the proliferation in Hep3B and HepG2 HCC cells. (G) The expression of Ki67, vimentin, and Snail were significantly downregulated, and the epithelial cell surface marker E-cadherin was upregulated in Hep3B and HepG2 cells that overexpressed WISP2.

Figure 2. Upregulation of WISP2 in HCC is related to inhibition of the malignant phenotype in vitro, while no difference in proliferation was found in subcutaneous tumorigenesis in vivo. (A) The expression of WISP2 was diverse in different tumour cell lines in the CCLE database. (B) The expression of WISP2 in 76% HCC cell lines, including Hep3B and HepG2, were low in CCLE database. (C) The expression of WISP2 was determined in Hep3B and HepG2, and confirmed using immunoblotting and immunocytochemistry. (D) Overexpression of WISP2 significantly inhibited the migration and invasiveness in Hep3B and HepG2 HCC cells. (E) Proliferation in Hep3B and HepG2 HCC cells that overexpress WISP2 or control cells was examined using a plate colony formation assay, and overexpression of WISP2 significantly impaired the colony formation. (F) Proliferation was assessed using a CCK8 assay, and overexpression of WISP2 significantly inhibited the proliferation in Hep3B and HepG2 HCC cells. (G) The expression of Ki67, vimentin, and Snail were significantly downregulated, and the epithelial cell surface marker E-cadherin was upregulated in Hep3B and HepG2 cells that overexpressed WISP2.