Fig. 2

RvD1 inhibits the CAFs-induced tumorgenicity of Hep3B cells along with reversing the mesenchymal and stem-like phenotypes. (a) Representative images of subcutaneous xenografts in nude mice implanted with Hep3B in the presence or absence of CAFs and treated with RvD1 (n = 6). (b) Xenografts weight (mg) and tumor sizes were monitored and undergone quantification analysis. n = 6, **P < 0.01 by ANOVA for tumor weight; *P < 0.05 or **P < 0.01 by repeated-measures ANOVA for tumor sizes. (c) Immunohistochemistry staining and the semi-quantification data of Ki-67, E-cadherin, Vimentin, Sox2 and Nanog in xenograft tissues from different groups. Magnification is × 400, the scale bar represents 20 μm. n = 6, *P < 0.05 or **P < 0.01 by ANOVA. (d) Schematic of establishing the orthotopic liver tumor model in nude mice using Luciferase-expressing Hep3B cells admixed with CAFs co-injection and administrated with RvD1 (n = 6 per group). (e) Representative BLI images of orthotopic liver tumor and metastasis in vivo were shown, and Luciferase signaling was analyzed. n = 6, **P < 0.01 by t test. (f) Representative hematoxylin and eosin–stained sections, and quantification analysis of tumor nodules in livers and metastasis nodules in lungs were shown. The scale bar represents 365 μm. n = 6, **P < 0.01 by t test