Fig. 6

ATO and ATRA cooperatively inhibit the population and self-renewal of TICs in TNBC. a, b ATO and ATRA cooperatively reduce the population of TICs in TNBCs. Human TNBC 231 (a) and 159 (b) cells were treated with ATO (1 µM) or ATRA (10 µM) or their combination, followed by FACS analysis of the TIC-enriched CD24⁻CD44⁺ population and ALDH⁺ population. c, d ATO and ATRA cooperatively inhibit the self-renewal of TICs in TNBCs. TNBC 231 (c) and 159 (d) cells were treated with ATO (1 µM) or ATRA (10 µM) or their combination, followed by serial mammosphere formation assay to measure their TIC self-renewal. Scale bar = 150 μm. e–g Pin1 KO using CRISPR reduce the population and self-renewal of TICs in TNBCs. Pin1 CRISPR KO and control 231 cells (e, g) or 159 cells (f) were subjected to FACS analysis of the TIC-enriched CD24⁻CD44⁺ population (e) and ALDH⁺ population (f) or serial mammosphere formation assay (g). Scale bar = 150 μm. h–j ATO and ATRA cooperatively inhibit the EMT of TNBC cells. TNBC 231 cells were treated with ATO (1 µM) or ATRA (10 µM) or their combination, followed by measuring the expression of E-cadherin (h), and slug, vimentin, and ZEB-1 (i) using real-time PCR or immunoblot (j). k, l ATO and ATRA cooperatively inhibit migration and invasion of TNBC cells. TNBC 231 cells were treated with ATO (1 µM) or ATRA (10 µM) or their combination, followed by assaying cell migration (k) and invasion (l) using Pin1 CRISPR KO cells as controls