Fig. 4

sFRP1 in HSCs accelerates HCC progression following chronic stress in vivo. a Serum NE levels in stressed or non-stressed mice were measured by ELISA. b, c Huh7 cells with or without LX2 cells were injected subcutaneously into the flanks of nude mice without or with chronic restraint stress. The tumor growth rates and tumor sizes are shown for mice in four groups: Huh7 (control), Huh7 (stress), Huh7 + LX2(control), and Huh7 + LX2(stress). d, e sFRP1, E-cadherin, N-cadherin, vimentin, snail, β-catenin c-Myc, cyclin D1, Nanog and Wnt16B expression levels in tumors from Huh7 + LX2(stress) versus Huh7 + LX2(control) groups were measured by western blot analysis, and sFRP1, cyclin D1, E-cadherin, N-cadherin, and β-catenin levels were validated using immunohistochemistry staining. f Huh7 + LX-2^{shRNA sFRP1} or Huh7 + LX-2^{shRNA NC} were injected subcutaneously into the flanks of nude mice with chronic restraint stress. Serum NE levels in mice subjected to chronic restraint stress were measured by ELISA. g, h The tumor growth rates and tumor sizes are shown for mice subjected to chronic restraint stress in two groups, Huh7 + LX-2 ^{shRNA sFRP1} versus Huh7 + LX-2^{shRNA NC}. i, j sFRP1, E-cadherin, N-cadherin, vimentin, snail, β-catenin c-Myc, cyclin D1, Nanog and Wnt16B expression levels in tumors in stressed mice from Huh7 + LX-2 ^{shRNA sFRP1} versus Huh7 + LX-2^{shRNA NC} groups were measured by western blot analyses, and sFRP1, cyclin D1, E-cadherin, N-cadherin, and β-catenin were validated using immunohistochemistry staining. *P < 0.05, **P < 0.01, *** P < 0.001