Fig. 6

CD36 mediates COMP induced MEK/ERK and PI3K/AKT pathways activation. a Cell viability after CD36 knockdown by shRNA was determined using CCK8 assay. The cell viability of every cell line with rCOMP+shCtl treatment was considered as control group. n = three independent repeats. P < 0.05 by ANOVA versus control. b and c HCC cells after knockdown of CD36 were subjected with transwell migration and invasion assays. The number of migrated or invaded cells was counted in five different fields. n = three independent repeats. P < 0.05 by t test versus control. d Photomicrographs were taken for orthotopic primary liver tumors formed by shCD36 + rCOMP or shCtl+rCOMP (left). Tumor volumes from each group (n = 5) were measured (right). P < 0.05 by t test versus shCtl+rCOMP. e Representative H&E-stained sections of the lung tissues from the two groups were showed in the left. Magnification × 200. A total of 10 random visual fields were chosen from different lung sections of each group, and pulmonary foci were quantified as the average number across the 10 visual fields per group (right). P < 0.05 by t test versus shCtl+rCOMP. f The expression of the indicated proteins in HCC cells after CD36 knockdown by shRNA compared with controls in Hep-3B and SMMC-7721 cells. CD36 knockdown was confirmed by Western blot. β-actin was used as a loading control. Western blot analysis was independently repeated for three times with similar results. g The expression of Ki67, CD36, E-cadherin, N-cadherin and vimentin in xenograft tumors from different groups were analyzed by immunohistochemistry. Representative images at × 200 magnification are shown. (*P < 0.05, **P < 0.01)