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Fig. 6 | BMC Cancer

Fig. 6

From: Selective mode of action of plumbagin through BRCA1 deficient breast cancer stem cells

Fig. 6

Model of BRCA1 defective BCSCs and response to anticancer agents. BRCA1 defective BCSCs are mostly positive for stem cell markers (Nuclear Oct 4 and membrane bound β-catenin) while BRCA1 wild type BCSCs shows expression of EMT markers (Snail, Slug, Vimentin) and mesenchymal marker (α-SMA). PB, an ROS inducer can cause DNA DSBs which cannot be effectively repaired in BRCA1 defective cells leading to apoptosis (unpublished data). Also, very high levels of HMOX1 expression in BRCA1 deficient condition as reported earlier, may cause apoptosis induction. ROS mediated DNA damages will be repaired and low levels of hypoxia created by PB can lead to low HMOX1 induction and further stem cell enrichment in BRCA1 wild type BCSCs. In addition to this, drug efflux will not happen as ABCG2 membrane translocation is hampered in presence of PB in BRCA1 defective mammospheres. Due to the presence of active ABCG2, drug efflux will also be high when treated with PB in BRCA1-wild type BCSCs. The same mechanism may be in action in both the conditions after CP treatment

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