Figure 8
A working model for tamoxifen-ERα36-mediated maintenance of breast CSCs. In ERα36+ breast cancer cells, 4-OHT or estrogen induces the nuclear translocation of ERα36 to regulate the transcriptional activity of ERα to increase ALDH1A1 expression. Elevated ALDH1A1 enriches breast CSCs as source of cancer metastasis. Inhibition of ALDH1 activity by DSF, DEAB or anti-ERα36 antibody eliminates ALDH1high breast CSCs.
