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. 2010 Dec 20;5(12):e15630. doi: 10.1371/journal.pone.0015630

Figure 3. BT-ICs are intrinsic chemoresistance independent of individual tumors and cell lines.

Figure 3

(A) The percentage of adriamycin resistant MCF-7 (AdrR/MCF-7) cells and epirubicin resistant SKBR3 (sk-3rd) cells with the phenotype of CD44+CD24− is significantly higher than parental MCF-7 line and SKBR3 line tested by FACS (42.38±4.80% vs. 1.82%±0.64%, 64.34±2.62% vs. 0.68%±0.16%, p<0.001). (B) FACS-sorted CD44+CD24− MCF-7 and CD44+CD24− AdrR/MCF-7 was about 10–60 fold higher resistant to adriamycin relative to the parental cells and non-CD44+CD24− cells. CD44+CD24− SK-3rd and primary cells were about 25 fold higher resistant to epirubicin relative to parental cells and non-CD44+CD24− cells by using cell viability assay. (C)Compared with non-BT-ICs, chemotherapy (adriamycin or epriubicin 0.5µg/ml for 24 hours) increased Annexin V positive cells of non-CD44+/CD24−cells, which derived from tumors with high or low proportion T-ICs, MCF-7, AdrR/MCF-7 and SK-3rd breast cancer cell lines containing different number of T-ICs (p<0.001). (D) MDR1 (multidrug resistance 1) and ABCG2(ATP-binding cassette sub-family G member 2) protein expression is both up-regulated in CD44+/CD24− cells from different cell lines and primary cells. All the experiments were repeated 3 times independently.