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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Hepatology. 2014 Feb 18;59(4):1435–1447. doi: 10.1002/hep.26790

Figure 3. Sorafenib treatment selectively increases tumor-associated fibrosis in HCC in an SDF1α/CXCR4 pathway-dependent manner.

Figure 3

A,B, Sorafenib significantly increased the collagen I content (A) and the number of α-SMA+ myofibroblasts (B) in orthotopic HCA-1 tumors implanted in mice with fibrotic livers. The analysis was performed using immunofluorescence in tumor tissue, and maker-positive area was normalized to the area of DAPI (nuclear stain) (N=5–7). C–D, Sorafenib treatment significantly increased the collagen I content (C and D) and the expression of α-SMA (D) (detected by Western blotting) in spontaneously arising HCCs (N=7–8). E, Representative images of immunofluorescence of Collagen I staining in spontaneous HCCs. Images are 636μm across. Addition of AMD3100 to sorafenib treatment prevented the increase in collagen I content and the number of α-SMA+ myofibroblasts in HCCs (A–E). F, In tumor-bearing mice, sorafenib significantly reduced the collagen I content in the surrounding liver tissue in mice with underlying liver fibrosis to levels comparable to those seen in livers from non-CCl4-treated mice (N=4–8). The number of random regions of interest used for quantification is shown in parentheses. *p<0.05; **p<0.01; Data are shown as mean ± SEM.