User Tools

Site Tools


phosphoinositide_3_kinase

Phosphoinositide 3 kinase

Phosphatidylinositol-4,5-bisphosphate 3-kinase (also called phosphatidylinositide 3-kinases, phosphatidylinositol-3-kinases, PI 3-kinases, PI(3)Ks, PI-3Ks or by the HUGO official stem symbol for the gene family, PI3K(s)) are a family of enzymes involved in cellular functions such as cell growth, proliferation, differentiation, motility, survival and intracellular trafficking, which in turn are involved in cancer.

The Phosphoinositide 3 kinase (PI3K)/Akt pathway is known to play a major role in angiogenesis. Studies have shown that the phosphatase and tensin homologue deleted on chromosome ten (PTEN), a tumor suppressor, is an antagonist regulator of the PI3K/Akt pathway and mediates angiogenesis by activating vascular endothelial growth factor (VEGF) expression.

PI3Ks are a family of related intracellular signal transducer enzymes capable of phosphorylating the 3 position hydroxyl group of the inositol ring of phosphatidylinositol (PtdIns).

The pathway, with oncogene PIK3CA and tumor suppressor PTEN, is implicated in insensitivity of cancer tumors to insulin and IGF1, in calorie restriction.


Current standard treatment for glioma patients is surgical removal followed by radiotherapy and adjuvant chemotherapy. Due to therapeutic resistance and tumor recurrence, efforts are ongoing to identify the molecules that are fundamental to regulate the tumor progression and provide additional methods for individual treatment of glioma patients. By studying the initiation and maintenance of glioma, studies focused on the targets of tyrosine kinase receptors including EGFR, PDGFR and other crucial signal pathways such as PI3K/AKT and RAS/RAF/MAPK pathway. Furthermore, recent advances in targeting immunotherapy and stem cell therapy also brought numerous strategies to glioma treatment 1).


PI3K/protein kinase B pathway may serve as a more reasonable molecular target for meningioma than EGFR 2).

1)
Lin L, Cai J, Jiang C. Recent advances in targeted therapy for glioma. Curr Med Chem. 2016 Dec 23. [Epub ahead of print] PubMed PMID: 28019637.
2)
Bujko M, Kober P, Tysarowski A, Matyja E, Mandat T, Bonicki W, Siedlecki JA. EGFR, PIK3CA, KRAS and BRAF mutations in meningiomas. Oncol Lett. 2014 Jun;7(6):2019-2022. Epub 2014 Apr 7. PubMed PMID: 24932282; PubMed Central PMCID: PMC4049666.
phosphoinositide_3_kinase.txt · Last modified: 2017/05/11 22:35 by administrador