Fig. 7: GPX4 promotes tumor progression and chemotherapy resistance in NPC by activating TAK1-JNK and IKK/NF-κB. | Cell Death & Differentiation

Fig. 7: GPX4 promotes tumor progression and chemotherapy resistance in NPC by activating TAK1-JNK and IKK/NF-κB.

From: EBV infection-induced GPX4 promotes chemoresistance and tumor progression in nasopharyngeal carcinoma

Fig. 7

A. The TAK1-NFκB/MAPK signaling pathway was examined in EBV-negative and EBV-positive NPC cells by immunoblotting. B Protein expression of TAK1 in EBV-negative and EBV-positive CNE2 cells transduced with siRNAs against endogenous TAK1. CCK-8 assay (C) and colony formation assay (D) in the indicated cells (n = 3). E. Dose–response curve for DPP, 5-FU, and TAX treatment in the indicated cells. F The TAK1-NFκB/MAPK signaling pathway was examined in the indicated stable cell lines treated with TAK1 siRNA by immunoblotting. G CCK-8 assay of CNE2 EBV-negative cells with stable overexpression of GPX4 treated with TAK1 siRNA (n = 4). H, I. Cell cycle analysis of the indicated cells by flow cytometry. J Colony formation of the indicated cells (n = 3). si Ctrl, negative control. Data are shown as the mean ± SD. **p < 0.01; ***p < 0.001; ****p < 0.0001. C, D and G, two-tailed unpaired t test.

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