NDLI: Phosphatidylinositol Phosphate 5-Kinase IÎ³ and Phosphoinositide 3-Kinase/Akt Signaling Couple to Promote Oncogenic Growth.

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Phosphatidylinositol Phosphate 5-Kinase IÎ³ and Phosphoinositide 3-Kinase/Akt Signaling Couple to Promote Oncogenic Growth.

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Phosphatidylinositol Phosphate 5-Kinase IÎ³ and Phosphoinositide 3-Kinase/Akt Signaling Couple to Promote Oncogenic Growth.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Anderson, Richard A. Thapa, Narendra Tan, Xiaojun Choi, Suyong Wise, Thomas
Description	Author Affiliation: Thapa N ( From the Molecular and Cellular Pharmacology Program, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin 53706.); Choi S ( From the Molecular and Cellular Pharmacology Program, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin 53706.); Tan X ( From the Molecular and Cellular Pharmacology Program, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin 53706.); Wise T ( From the Molecular and Cellular Pharmacology Program, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin 53706.); Anderson RA ( From the Molecular and Cellular Pharmacology Program, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin 53706 raanders@wisc.edu.)
Abstract	The assembly of signaling complexes at the plasma membrane is required for the initiation and propagation of cellular signaling upon cell activation. The class I PI3K and the serine/threonine-specific protein kinase Akt signaling pathways (PI3K/Akt) are often activated in tumors. These pathways are initiated by the generation of phosphatidylinositol 3,4,5-triphosphate (PIP3) by PI3K-mediated phosphorylation of phosphatidylinositol 4,5-biphosphate (PIP2), synthesized by phosphatidylinositol 4-phosphate 5-kinase (PIPKI) enzymes. The mechanism of how tumor cells recruit and organize the PIP2-synthesizing enzymes with PI3K in the plasma membrane for activation of PI3K/Akt signaling is not defined. Here, we demonstrated a role for the phosphatidylinositol 4-phosphate 5-kinase IÎ³ (PIPKIÎ³) in PI3K/Akt signaling. PIPKIÎ³ is overexpressed in triple-negative breast cancers. Loss of PIPKIÎ³ or its focal adhesion-targeting variant, PIPKIÎ³i2, impaired PI3K/Akt activation upon stimulation with growth factors or extracellular matrix proteins in different tumor cells. PIPKIÎ³i2 assembles into a complex containing Src and PI3K; Src was required for the recruitment of PI3K enzyme into the complex. PIPKIÎ³i2 interaction with Src and its lipid kinase activity were required for promoting PI3K/Akt signaling. These results define a mechanism by which PIPKIÎ³i2 and PI3K are integrated into a complex regulated by Src, resulting in the spatial generation of PIP2, which is the substrate PI3K required for PIP3 generation and subsequent Akt activation. This study elucidates the mechanism by which PIP2-generating enzyme controls Akt activation upstream of a PI3K enzyme. This pathway may represent a signaling nexus required for the survival and growth of metastasizing and circulating tumor cells in vivo.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	30
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-07-24
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Neoplasms Genetics Phosphatidylinositol 3-Kinases Biosynthesis Phosphotransferases (Alcohol Group Acceptor) Proto-Oncogene Proteins C-akt Cell Proliferation Gene Expression Regulation, Neoplastic MCF-7 Cells Metabolism Pathology Phosphatidylinositol Phosphates Phosphatidylinositols Signal Transduction Transcriptional Activation Src-Family Kinases Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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