Fig. 1

CAFs derived from HNC are innately resistant to cisplatin. a Immunofluorescence staining for α-SMA, FAP, and FSP1 expression of NFs and CAFs (scale bar, 20 μm). b Western blot analysis of α-SMA, FAP, and FSP1 protein levels in six paired NFs and CAFs. c NFs, CAFs, and HNC cells were treated with or without 10 μM cisplatin for 8 days, and cell viability was measured to obtain percent cell survival and was normalized to that of control cells. d NFs, CAFs, and HNC cells were treated with or without 10 μM cisplatin for 24 h, and cell viability was detected to calculate the percentage of proliferating cells during cisplatin treatment. e The percentage of surviving CAFs (CAF3) and cisplatin-resistant HN4-res cells, which exhibit similar proliferation retention rates, upon 10 μM cisplatin treatment for 8 days. f, g Western blot analysis of MRP2, ATP7B, CTR1, XIAP, ERCC1, ERCC4, GSTK1, and Bcl-2 protein levels in NFs, CAFs, CAL 27, SCC-25, HN4, and HN4-res cells. The band intensity was assessed. (ns, no significant difference; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001)