Fig. 2: PRMT5 promotes cisplatin chemoresistance by regulating efficient DNA repair in BCSCs.
From: PRMT5-regulated splicing of DNA repair genes drives chemoresistance in breast cancer stem cells
A Mammosphere assay of cisplatin-treated MCF7-shCTRL or -shPRMT5 cells. B Mammosphere assay of cisplatin and GSK591-treated MCF7 cells. C Mammosphere assay of cisplatin-treated MCF7-shPRMT5 cells reconstituted with wildtype (WT) or methyltransferase dead (MD) PRMT5. D PARP1-cleavage assay of cisplatin and GSK591-treated AR BCSCs. White bar indicates bulk cells treated with 50 μM cisplatin. E Mammosphere assay of tumour-derived MCF7 cells treated with cisplatin and GSK591 ex vivo (n = 15). F 53BP1 foci analysis of cisplatin-treated AR BCSCs isolated from GSK591-treated MCF7 cells. Foci were scored in mitosin-positive cells. G Alkaline comet assay of MCF7 cells treated with GSK591 and cisplatin. AR BCSCs were isolated and treated with 30 Gy IR (bar = median). Unless otherwise stated n = 3; mean ± SEM; Student’s t test (two-sided, equal variance).
