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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 7. Sorafenib induces a modest growth delay in HCC, and CXCR4 inhibition or blockade of Gr-1 synergize with sorafenib treatment by increasing cell apoptosis.

Figure 7

A, Sorafenib (SOR) treatment induces a minor but significant delay in orthotopic HCC models after 14 days of treatment. HCA-1 tumor growth was delayed by sorafenib in syngeneic C3H mice with underlying liver fibrosis (N=6–14 mice per group). Whereas treatment with the CXCR4 inhibitor AMD3100 (AMD) had no effect as monotherapy, AMD3100 with sorafenib induces a more significant tumor growth delay. B, Representative images of immunofluorescence TUNEL in HCA-1 tumors. Images are 636μm across. C, Cell apoptosis, measured by TUNEL, increased after sorafenib treatment in HCA-1 tumors (N=6–11). D, Representative images of immunofluorescence of TUNEL in spontaneous HCCs. Images are 636μm across. E, Cell apoptosis, measured by TUNEL, increased after sorafenib treatment in spontaneously arising HCCs in Mst1−/− Mst2F/− transgenic mice (N=6–11). Cell apoptosis was significantly increased when sorafenib treatment was combined with AMD3100 in both tumor models. F, Combining anti-Gr-1 antibodies with sorafenib treatment induced a significant tumor growth delay of orthotopic HCA-1 tumors growing in mice with liver fibrosis (N=7–13 mice per group). Data are presented as mean ± SEM; *P<0.05, **P<0.01.