PI3K/Akt signaling pathway is involved in several human cancers

The PI3K/Akt signaling pathway is involved in several human cancers. When bound, growth factor (GF) receptor tyrosine kinases (RTK) recruit PI3K, a heterodimer with both a regulatory p85 and a catalytic p110 subunit. PI3K phosphorylates PIP2 creating PIP3, which then activates Akt. Once phosphorylated by PIP3, Akt affects many cellular processes either directly (dark lines) or indirectly (dashed lines) through the regulation of downstream mediators. By inhibiting proteins that promote apoptosis, such as p53, Bad, and the FOXO family of forkhead transcription factors, Akt furthers cell survival. Akt also regulates survival by stimulating pro-survival proteins like NF-κB. Indirect activation of the mTOR pathway by Akt increases protein synthesis and cell growth, while the triggering of eNOS overexpression is thought to contribute to tumor angiogenesis. In addition, Akt is indirectly involved in the control of cell cycle progression through interactions with FOXO transcription factors, GSK3, Myc, and subsequent effects on cyclin D1 and p27KIP1 (not depicted).

Publication

The Phosphatidylinositol 3-Kinase/Akt Signaling Pathway in Medullary Thyroid Cancer. () Susan C. Pitt, et al. Surgery. ;144(5):721-724. Figure: F1. All organisms Drosophila melanogaster Homo sapiens

Disease mentions