Fig. 5: IL-6-induced BECN1 Y333 phosphorylation promotes cancer chemotherapy resistance.

a CCK-8 assays for cell viability of SW48 cells separately pretreated with DMEM or IL-6 (20 ng/ml) for 8 h in the presence of DMSO, 5-Fu (800 μM), or OXA (100 μM) for 36 h. **P < 0.01, ***P < 0.001 (n = 3 independent experiments). b Western blot analyses for cleaved caspase-3 and cleaved PARP1 in SW48 cells separately pretreated with DMEM or IL-6 (20 ng/ml) for 8 h in the presence of DMSO, 5-Fu (800 μM) or OXA (100 μM) for 36 h (n = 3 independent experiments). c CCK-8 assays for cell viability of SW48 cells separately pretreated with DMEM or IL-6 (20 ng/ml) for 8 h in the presence of CQ (25 μM), 5-Fu (800 μM) or OXA (100 μM) for 36 h. *P < 0.05, **P < 0.01, ***P < 0.001 (n = 3 independent experiments) d Western blot analyses for cleaved caspase-3 and cleaved PARP1 in SW48 cells separately pretreated with DMEM or IL-6 (20 ng/ml) for 8 h in the presence of CQ (25 μM), 5-Fu (800 μM), or OXA (100 μM) for 36 h. (n = 3 independent experiments). e In vivo CRC xenografts derived from CT26 cells were treated with IL-6, 5-Fu, or OXA. Quantification of tumor weights from the different CRC xenografts is shown. **P < 0.01, ***P < 0.001. f Tumor volumes at the experimental endpoint were quantified in CT26 cell xenografts. g The apoptotic index was quantified for the different CRC xenografts. **P < 0.01, ***P < 0.001. h–j In vivo CRC xenografts derived from CT26 cells and CT26-Becn1-KO cells separately expressing a vector control (Vector), Becn1 WT, Becn1 Y3331F, or Becn1 Y3331 were treated with DMSO, 5-Fu or OXA. Tumor weights (h), tumor volumes (i), and apoptotic index (j) quantified at the experimental endpoint are shown (n = 5 mice per genotype). **P < 0.01, ***P < 0.001. NS not significant. In (a, c, e, g, h and j), the values are presented as the means ± SEM; p values (Student’s t test, two-sided) with control or different indicated groups are shown. Source data are provided in the Source Data file.