PI3K-p110α mediates the oncogenic activity induced by loss of the novel tumor suppressor PI3K-p85α
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چکیده
منابع مشابه
PI3K-p110α mediates the oncogenic activity induced by loss of the novel tumor suppressor PI3K-p85α.
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 hu...
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The PI3K (phosphoinositide 3-kinase) pathway is commonly activated in cancer as a consequence of inactivation of the tumour suppressor PTEN (phosphatase and tensin homologue deleted on chromosome 10), a major negative regulator of PI3K signalling. In line with this important role of PTEN, mice that are heterozygous for a PTEN-null allele (PTEN+/− mice) spontaneously develop a variety of tumours...
متن کاملRegulation of the PI3K pathway through a p85α monomer–homodimer equilibrium
The canonical action of the p85α regulatory subunit of phosphatidylinositol 3-kinase (PI3K) is to associate with the p110α catalytic subunit to allow stimuli-dependent activation of the PI3K pathway. We elucidate a p110α-independent role of homodimerized p85α in the positive regulation of PTEN stability and activity. p110α-free p85α homodimerizes via two intermolecular interactions (SH3:proline...
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Phosphatidylinositol 3-kinase (PI3K) plays an important role in cell growth, proliferation and motility. The regulatory subunit, p85α, is the most abundantly expressed regulatory isoform of PI3K and is essential for the activation of PI3K. PI3K p85α is often over-expressed in colorectal cancer (CRC) cells, but its role in the migration and invasion of CRC remains unclear. In this study, lentivi...
متن کاملDirect engagement of the PI3K pathway by mutant KIT dominates oncogenic signaling in gastrointestinal stromal tumor.
Gastrointestinal stromal tumors (GISTs) predominantly harbor activating mutations in the receptor tyrosine kinase KIT. To genetically dissect in vivo the requirement of different signal transduction pathways emanating from KIT for tumorigenesis, the oncogenic KitV558Δ mutation was combined with point mutations abrogating specific phosphorylation sites on KIT. Compared with single-mutant KitV558...
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ژورنال
عنوان ژورنال: Proceedings of the National Academy of Sciences
سال: 2017
ISSN: 0027-8424,1091-6490
DOI: 10.1073/pnas.1704706114