Figure 6.
The potential mechanism of action of miR-145 and miR-210 in cancer cells. PI3k/AKT signaling is often constitutively activated in cancer. Inactivation of FOXO1 and subsequent inhibition of miR-145 expression by the PI3K/AKT pathway favors cell survival, proliferation, and expansion of the CSC population and increases self-renewal and tumorigenic capacity. Activation of STAT3 induces cancer cell survival by inducing the expression of c-Myc. miR-210 inhibits SOCS1 and activates the STAT3 pathway favoring cell survival.