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Article

PI3K-p110α mediates the oncogenic activity induced by loss of the novel tumor suppressor PI3K-p85α.

Proceedings of the National Academy of Sciences of the United States of America - 3 Jul 2017

Thorpe Lauren M, Spangle Jennifer M, Ohlson Carolynn E, Cheng Hailing, Roberts Thomas M, Cantley Lewis C, Zhao Jean J

Abstract excerpt

Mutation or loss of the p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3K) is emerging as a transforming factor in cancer, but the mechanism of transformation has been controversial. Here we find that hemizygous deletion of the PIK3R1 gene encoding p85α is a frequent event in breast cancer, with PIK3R1 expression significantly reduced in breast tumors. PIK3R1 knockdown transforms human mammary...

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Share to Class I Phosphatidylinositol 3-Kinases
Share to Class Ia Phosphatidylinositol 3-Kinase

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Enzyme Activation

Share to Epithelial Cells

Share to Gene Expression Regulation, Enzymologic

Share to Gene Knockdown Techniques

Share to Intercellular Signaling Peptides and Proteins

Share to Mammary Glands, Animal

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Identifiers

PMID: 28630349
DOI: 10.1073/pnas.1704706114
PMCID: PMC5502636

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PI3K-p110α mediates the oncogenic activity induced by loss of the novel tumor suppressor PI3K-p85α.PMID 28630349Read ↗

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