Title : TGF-β1-activated cancer-associated fibroblasts promote breast cancer invasion, metastasis and epithelial-mesenchymal transition by autophagy or overexpression of FAP-α.

Pub. Date : 2021 Jun

PMID : 33741330






3 Functional Relationships(s)
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1 Modulation of autophagy by rapamycin, 3-methyladenine or ATG-5 knockdown regulated the expression of CAFs markers, suggesting a role of autophagy in the tumor promotion mechanism of TGF-beta1-induced CAFs activation. 3-methyladenine transforming growth factor beta 1 Homo sapiens
2 We demonstrated that TGF-beta1-activated CAFs promote tumor invasion, pulmonary metastasis and EMT, which act through autophagy and overexpression of FAP-alpha in both models, while autophagy inhibitor 3-methyladenine blocked these effects induced by TGF-beta1-activated CAFs. 3-methyladenine transforming growth factor beta 1 Homo sapiens
3 We demonstrated that TGF-beta1-activated CAFs promote tumor invasion, pulmonary metastasis and EMT, which act through autophagy and overexpression of FAP-alpha in both models, while autophagy inhibitor 3-methyladenine blocked these effects induced by TGF-beta1-activated CAFs. 3-methyladenine transforming growth factor beta 1 Homo sapiens