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. 2021 Apr 6;9:631931. doi: 10.3389/fcell.2021.631931

FIGURE 5.

FIGURE 5

CAFs driven by SULF2 induced HCC EMT phenotype via upregulating SNAI1 by activating SDF-1/CXCR4 signaling. (A) By western immunoblotting assay, it was found that Hep3B LX2 SULF2 cells had significantly more expression of SNAI1, N-cadherin, and Vimentin and less E-cadherin expression than Hep3B LX2 Vector cells, while co-culture with LX2 SULF2 cells did not alter the expression of E-cadherin, SNAI1, N-cadherin, and Vimentin after treatment of AMD3100. Cell fractions: Hep 3B cells (the protein was extracted from total cells). (B) As assessed by wound healing assay, the migration ability of Hep3B cells was found to be accelerated by co-culture with LX2 SULF2 cells, which was weakened by treatment of AMD3100. (C) Transwell invasion assay showed that co-culture with LX2 SULF2 cells consolidated the invasion capacity of Hep3B cells and AMD3100 treatment attenuated the regulatory effect of co-culture with LX2 SULF2 cells on the Hep3B cell invasion ability. CAF, carcinoma-associated fibroblast; SULF2, sulfatase 2; HCC, hepatocellular carcinoma; EMT, epithelial-to-mesenchymal transition.