Figure 7. Sources of EPO and proposed mechanism of EPO-promoting breast TIC self renewal.
Intratumoral EPO may be derived from several intratumoral cells including stromal cells, cancer-associated endothelial cells, and breast cancer cells as well as exogenous administration. Intratumoral EPO activates EPO-R present on breast TICs that subsequently activates JAK/STAT signaling promoting TIC self renewal and stemness. Potential effects of EPO on the non-TIC fraction will need to be investigated. The JAK inhibitor TG101348 inhibits JAK/STAT signaling and EPO-dependent breast TIC self renewal.
