Fig. 7: Schematic diagram depicting the oxidative stress-USP29-Snail1 regulation axis of cancer cells in responsive to chemotherapies.

Our current working model proposes that lung adenocarcinoma cells display their intrinsic capabilities of rewiring transcriptional circuitry to increase USP29 expression in responsive to oxidative stresses incurred by chemotherapeutic agents. USP29 upregulation leads to the stabilization of Snail1, which acts as the master regulator to enable the expression of a range of mesenchymal genes. As a consequence, this oxidative stress-USP29-Snail1 regulation axis confers cancer cells enhanced stemness and chemoresistance. TF transcription factor, Ub ubiquitin, E3 ubiquitin E3 ligase.