Fig. 4: VEGF-A secretion induced by MCL-1 inhibition in bCAFs involves BAX/BAK activity. | Cell Death & Disease

Fig. 4: VEGF-A secretion induced by MCL-1 inhibition in bCAFs involves BAX/BAK activity.

From: MCL-1 as a molecular switch between myofibroblastic and pro-angiogenic features of breast cancer-associated fibroblasts

Fig. 4

A BAX and BAK protein expression level in bCAFs after gene silencing evaluated using Western blots. Actin expression was used as loading control (n = 3). B VEGF-A secretion analysed by ELISA in bCAFs CM expressing or not BAX/BAK (bCAFsgBAX/BAK) after 18 h of treatment with MCL-1 inhibitor (S63845 500 nM) or not (n = 3). Two-way ANOVA, **P < 0.01; ns non-significant. C Cytochrome C released in bCAFs after 18 h of treatment with S63845 (500 nM). Co-treatment with S63845 (500 nM) and A1331852 (BCL-xL inh., 100 nM) served as positive control of Cyto C release (n = 3). Student t-test, **P < 0.01, ****P < 0.0001. D VEGF-A secretion analysed by ELISA in bCAFs CM after 18 h of treatment with MCL-1 inhibitor (S63845 500 nM) in combination with pan-caspase inhibitor (Q-VD-OPH 5 µM) (n = 5). Two-way ANOVA, *P < 0.05; ns non-significant.

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