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. Author manuscript; available in PMC: 2015 Jan 29.
Published in final edited form as: Curr Drug Targets. 2014 Jan;15(1):65–79. doi: 10.2174/1389450114666140106100909

Fig. 1. PTEN exhibits tumor suppressive functions in the cytoplasm and nucleus.

Fig. 1

The phosphatidylinositol 3-kinase (PI3K) pathway regulates cancer cell growth and survival. This pathway is activated by ligand binding to receptor tyrosine kinases (RTKs) and/or G protein coupled receptors (GPCRs). PI3K is then recruited to the membrane where it phosphorylates phosphatidylinositol (4,5)-bisphosphate (PIP2) to produce phosphatidylinositol (3,4,5)-trisphosphate (PIP3), leading to activation of several signaling cascades including AKT/mTORC1. Cytoplasmic PTEN negatively regulates this pathway by dephosphorylating PIP3 at its D3 position. Nuclear PTEN promotes chromosome stability and regulates DNA double-strand break repair. Red star indicates a potential therapeutic target for which a drug(s) is in development.