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Fig. 6 | Journal of Translational Medicine

Fig. 6

From: CD36 promotes the epithelial–mesenchymal transition and metastasis in cervical cancer by interacting with TGF-β

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. bd 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

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