Fig. 7

Schematic depicting the molecular mechanism of Api5-mediated transformation of breast epithelial cells. Api5 through FGF2 (High Molecular weight—nuclear localised) led to activation of FGFR1 growth factor receptor signaling. During the early days of morphogenesis, overexpression of Api5 led to elevated proliferation via the PDK1- Akt/cMYC pathway thus, aiding in the transformation of breast epithelial cells. cMYC is known to promote EMT and anchorage-independent growth was also observed in Api5 OE MCF10A cells. Further, during the later days of morphogenesis, FGF2 signalling activated ERK-mediated Bim degradation, thereby inhibiting apoptosis, and supporting sustained proliferation. Both the signalling cascades can contribute to the partial-EMT state observed in Api5 OE MCF10A cells. Thick lines show signalling mechanisms revealed from experiments conducted in this study while dotted lines represent signalling mechanisms obtained from published literature