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The epithelial-to-mesenchymal transition (EMT) program is crucial for the epithelial cancer progression and fibrotic diseases. Our previous work has demonstrated that p66 Shc , a focal adhesion-associated adaptor protein, is frequently downregulated in lung cancers and its depletion promotes metastasis behavior through anoikis resistance. However, mechanism underlying loss of p66 Shc  and EMT response is not fully understood. Here, we showed that p66 Shc  deficiency enhanced the expression of ZEB1, the known mesenchymal transcription factor and consequently increased Vimentin, and decreased epithelial markers of E-cadherin and  β -catenin. p66 Shc  depletion also increased cell invasion and migration. In addition, ChIP and luciferase assays showed that these effects were directly mediated by ZEB1 repression of p66 Shc  promoter. Thus, our findings define a critical role of p66 Shc  in the suppression of fibrotic EMT response with a negative feedback loop between p66 Shc  and ZEB1 in lung epithelial cancer cells.

Negative feedback loop between p66Shc and ZEB1 regulates fibrotic EMT response in lung cancer cells