Fig. 5: The combination treatment induces apoptosis by downregulating MCL-1 via p38-MAPK signaling. | Cell Death & Disease

Fig. 5: The combination treatment induces apoptosis by downregulating MCL-1 via p38-MAPK signaling.

From: Targeted activation of GPER enhances the efficacy of venetoclax by boosting leukemic pyroptosis and CD8+ T cell immune function in acute myeloid leukemia

Fig. 5

A Western blotting of MCL-1 in the same treated cells as in Fig. 3D–F. B Western blot analysis of MCL-1 in the cell lines pretreated with CHX (10 μg/ml) for 1 h and then treated with 1 μM G-1 at indicated time points. C Western blotting of MCL-1 in the cell lines treated with 1 μM G-1 for 24 h, with or without pretreatment with MG-132(1 μM) for 1 h. Ubiquitination analysis of the ubiquitinated MCL-1 level. D KEGG analysis of these significant gene signatures from corresponding NES. E Western blot analysis of MAPK downstream signaling in the cell lines treated with 1 μM G-1 for the corresponding times. F IF staining of the p-p38 and p-JNK (green). The nucleus was stained blue with DAPI (scale bar, 50 μm). G Western blot analysis of MCL-1 in the cell lines pretreated with 1 μM SB203580 (SB) or 5 μM SP600125 (SP) for 1 h and then exposed to 1 μM G-1 for 24 h. H Western blot analysis of MCL-1 in the cell lines pretreated with 1 μM SB for 1 h, followed with G-1 and VEN, alone or in combination for 24 h. I IP analysis followed by western blot of BIM binding proteins in the cells treated with G-1 and VEN, alone or in combination for 24 h. J FCM of apoptosis in the cells infected with sh RNA targeting MCL-1 pretreated with 1 μM SB for 1 h, and then exposed to G-1 and VEN, alone or in combination for 24 h. The data are expressed as the mean ± SD (n = 3). **p < 0.01. ns, not significant.

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