Figure 7. A schematic diagram of the BMX-mediated AKT and STAT3 pathway activation in human cervical cancer cells.

Upon stimuli, BMX, as well as AKT, was activated by tyrosine phosphorylation of downstream PI3K via binding to PIP3 through the PH domain [16, 33, 34]. BMX could activate the phosphorylation of AKT and STAT3. Using three specific inhibitors of the AKT/mTOR and STAT3 pathways, the allosteric AKT inhibitor MK-2206, mTOR inhibitor rapamycin, and STAT3 inhibitor cryptotanshinone, cell proliferation was further inhibited in BMX-knockdown groups. These findings provide new evidence of the BMX function in cell proliferation and carcinogenesis of cervical cells through the PI3K/AKT/mTOR and STAT3 pathways.