Copyright
©The Author(s) 2019.
World J Clin Cases. Aug 6, 2019; 7(15): 1937-1953
Published online Aug 6, 2019. doi: 10.12998/wjcc.v7.i15.1937
Published online Aug 6, 2019. doi: 10.12998/wjcc.v7.i15.1937
Figure 1 The crosstalk between estrogen receptor and growth factor receptor intracellular signaling pathways.
Growth factor receptors (GFRs) activate the downstream PI3K/AKT/mTOR signaling pathway and the Cyclin D1/CDK4/6 complex, while the ER-E2 complex has the same effect[79]. The Cyclin D1/CDK4/6 complex drives cell proliferation by inducing Rb phosphorylation and promotes cell cycle from G1 phase to S phase in the nucleus[80]. Targeted agents against the CDK4/6 pathway and the PI3K/AKT/mTOR pathway can trigger cell cycle arrest and control tumor progression. ER: Estrogen receptor; GFR: Growth factor receptor; CDK4/6: Cyclin-dependent kinase; PI3K: Phosphatidylinositol 3-kinase; PIP2: Phosphatidylinositol 4,5-biphosphate; PIP3: Phosphatidylinositol triphosphate; mTOR: Mammalian target of rapamycin; Rb: Retinoblastoma protein.
- Citation: Yao LT, Wang MZ, Wang MS, Yu XT, Guo JY, Sun T, Li XY, Xu YY. Neoadjuvant endocrine therapy: A potential strategy for ER-positive breast cancer. World J Clin Cases 2019; 7(15): 1937-1953
- URL: https://www.wjgnet.com/2307-8960/full/v7/i15/1937.htm
- DOI: https://dx.doi.org/10.12998/wjcc.v7.i15.1937