Fig. 5
From: Loss of exosomal miR-3188 in cancer-associated fibroblasts contributes to HNC progression
BCL2 overexpression reverse the effects of suppression of miR-3188. a Immunoblotting analysis of endogenous BCL2, cleaved PARP, cyclin D1, BAX and cleaved caspase3 protein expression levels in HN4 and HN30 cells treated with miR-3188 mimics. β-Tubulin served as a loading control. b CM was collected from CAFs overexpressed miR-3188 and used to treat HNC cells for 48 h, then BCL2, cleaved PARP, cyclin D1, BAX and cleaved caspase3 protein expression levels were assessed using western blotting. MTT assay (c, d), EdU assay (e, f), colony formation assay (g, h), apoptosis analysis (i) and cell cycle analysis (j) of HNC cells were performed after transfected with miR-3188 mimics, miR-3188 mimics plus ectopic BCL2, siBCL2 and siBCL2 plus miR-3188 inhibitor (Scale bar = 40 μm). (NC, negative control. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001)