Fig. 7: ABCG1 confers cancer cell stemness and cisplatin resistance through upregulation of CD326.

Inhibition rates of various cell lines treated with cisplatin in terms of silencing or overexpression of ECM1, ABCG1, and hnRNPLL (a, data are presented as mean ± SD, n = 3 biologically independent repeats, two-tailed t-test was calculated between A8i-ABCG1 and A8i <upper> or A8i-A <lower>) and IC50 values (b, data are presented as mean ± SD, n = 3 biologically independent repeats, two-tailed t-test) of cisplatin in these cells as detected by CCK-8 assay. c Expression of stem cell transcription factors detected by WB analysis in ECM1-, ABCG1-, and hnRNPLL-silenced or -overexpressing cells. d Numbers of CD117+ and CD326+ cells (left panel, data are presented as ± SD, n = 3 biologically independent repeats, two-tailed t-test) and cisplatin inhibition rates (right panel, data are presented as ± SD, n = 3 biologically independent repeats) after three selection-and-culture cycles from CD117 + cells. e Numbers of CD117 + and CD326 + cells (left panel, data are presented as mean ± SD, n = 3 biologically independent repeats, two-tailed t-test) and cisplatin inhibition rates (right panel, data are presented as mean ± SD, n = 3 biologically independent repeats, two-tailed t-test was calculated between CD117+ and CD326+ <upper> or CD117+/CD326+ and CD117−/CD326−) after four selection-and-culture cycles from CD326+ cells. f A low concentration of cisplatin enriches CD326+ cells to increase cancer cell stemness. Data are presented as mean ± SD, n = 3 biologically independent repeats, two-tailed t-test. g Cisplatin treatment upregulates the expression of stem cell transcription factors in CD326+ cells.