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In Vitro Evaluation of Oncogenic Transformation in Human Mammary Epithelial Cells
09:44

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Published on: September 24, 2020

Class I PI3K in oncogenic cellular transformation.

L Zhao1, P K Vogt

  • 1Division of Oncovirology, Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA. leyna@scripps.edu

Oncogene
|September 17, 2008
PubMed
Summary
This summary is machine-generated.

Class I phosphoinositide 3-kinase (PI3K) enzymes, particularly the p110 alpha isoform, are frequently mutated in cancer, leading to oncogenic gain-of-function. Targeting these PI3K isoforms offers promising therapeutic strategies for cancer treatment.

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08:18

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Published on: December 31, 2014

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Class I phosphoinositide 3-kinases (PI3Ks) are dimeric enzymes with catalytic (p110 alpha, beta, gamma, delta) and regulatory (p85, p101) subunits.
  • PI3Ks are crucial in human cancer, with frequent mutations in PIK3CA (encoding p110 alpha) observed in common cancers.
  • Mutations in p110 alpha confer oncogenic gain-of-function through altered enzymatic and signaling activities.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the gain of function in mutant p110 alpha.
  • To explore the oncogenic potential of different PI3K isoforms in cancer.
  • To highlight PI3K isoforms as drug targets for cancer therapy.

Main Methods:

  • Analysis of structural and genetic data related to PI3K mutations.
  • Investigating the impact of mutations on regulatory subunit interactions (p85, Ras).
  • Assessing the oncogenic potential of wild-type and mutant PI3K isoforms in cell culture and animal models.

Main Results:

  • Mutant p110 alpha exhibits gain-of-function, promoting oncogenesis via mechanisms independent of p85 binding or Ras interaction.
  • Non-alpha PI3K isoforms, while lacking cancer-specific mutations, show differential expression and oncogenic potential upon overexpression.
  • Development of isoform-selective PI3K inhibitors is ongoing, with a focus on targeting cancer-specific p110 alpha mutants.

Conclusions:

  • PI3K isoforms, especially p110 alpha, are critical in cancer development and progression.
  • Understanding the distinct mechanisms of PI3K isoform activation is key for targeted cancer therapies.
  • Targeted inhibition of specific PI3K isoforms and mutants represents a significant frontier in drug development for cancer treatment.