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. 2023 Jul 25;10(27):2206878. doi: 10.1002/advs.202206878

Figure 2.

Figure 2

SQLE depletion restores cisplatin sensitivity in cisplatin‐resistant HNSCC cells both in vitro and in vivo. a,b) Colony formation potential of SCC‐1cisR, SCC‐23cisR, and CAL‐27cisR cells with SQLE depletion, with or without cisplatin treatment (n = 4). Cisplatin concentrations: SCC‐1cisR, 8 µg mL−1; SCC‐23cisR, 5 µg mL−1; CAL‐27cisR, 8 µg mL−1. SQLE knockdown efficiency determined by western blotting. c) Apoptosis rate of SCC‐1cisR and SCC‐23cisR cells with SQLE depletion in the presence or absence of cisplatin (n = 4). d) Cell viability of SCC‐1cisR, SCC‐23cisR, and CAL‐27cisR cells with SQLE depletion following dose‐gradient cisplatin exposure (n = 4). e–g) Effect of SQLE depletion on tumor growth in SCC‐1cisR cells with or without cisplatin treatment. Mice were treated with vehicle control or cisplatin (5 mg kg−1 i.p. twice per week) starting 1 week after tumor cell inoculation (n = 6). Tumor volume and animal health status were monitored. h) IHC scores of Ki‐67 and CD44 in xenograft tumor tissues with SQLE knockdown, in the presence or absence of cisplatin (n = 6). Scale bar: 100 µm. Data were presented as mean ± SD. ***p < 0.001 for one‐way ANOVA test.