Fig. 6

Western blots were used to analyze the association between CD36 and TGF-β-mediated EMT. a Knockdown of CD36 led to a dramatic increase in E-cadherin and decrease in vimentin, slug, snail, and twist both in SiHa and HeLa cells. Conversely, after transfected with exogenous CD36, these phenotypes were reversed. TGF-β treatment attenuated E-cadherin expression and enhanced the expression levels of CD36, vimentin, slug, snail, and twist in si-SiHa, si-HeLa, and C33a–CD36 cells. TGF-β regulated EMT markers though CD36. b–d Under the condition with or without TGF-β, expression levels of CD36, E-cadherin, vimentin, slug, snail, and twist in si-SiHa, si-HeLa, and C33a–CD36 cells (*P < 0.05, **P < 0.01). e CD36 also regulated expression levels of TGF-β