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Updated: May 12, 2026

Identification of Inositol Phosphate or Phosphoinositide Interacting Proteins by Affinity Chromatography Coupled to Western Blot or Mass Spectrometry
08:07

Identification of Inositol Phosphate or Phosphoinositide Interacting Proteins by Affinity Chromatography Coupled to Western Blot or Mass Spectrometry

Published on: July 26, 2019

Phosphoinositide 3-kinase and INPP4B in human breast cancer

Micka C Bertucci1, Christina A Mitchell

  • 1Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia.

Annals of the New York Academy of Sciences
|April 5, 2013
PubMed

Insights

The PI3K/Akt pathway is often overactive in cancers like breast cancer. INPP4B, a newly identified tumor suppressor, inhibits this pathway and may be crucial in regulating various cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is frequently dysregulated in numerous human cancers.
  • This pathway plays a critical role in cell proliferation, survival, and metabolism, making it a key target in cancer research.
  • Aberrant PI3K/Akt signaling contributes to tumorigenesis and progression in various malignancies, including breast cancer.

Purpose of the Study:

  • To review the emerging role of Inositol Polyphosphate-4-Phosphatase Type II B (INPP4B) as a tumor suppressor in breast cancer.
  • To discuss the inhibitory effect of INPP4B on the PI3K signaling pathway.
  • To explore the potential of INPP4B as a significant regulator in a broader range of cancers.

Main Methods:

  • Literature review of recent studies on PI3K/Akt signaling and INPP4B.
  • Analysis of the molecular mechanisms by which INPP4B regulates PI3K signaling.
  • Comparative analysis of INPP4B expression and function across different cancer types.

Main Results:

  • INPP4B acts as a negative regulator of the PI3K signaling pathway.
  • Loss or mutation of INPP4B is associated with increased PI3K signaling and tumor progression.
  • INPP4B demonstrates tumor-suppressive functions in preclinical models of breast cancer.

Conclusions:

  • INPP4B is an emerging tumor suppressor with a critical role in inhibiting PI3K signaling.
  • The dysregulation of INPP4B is implicated in the pathogenesis of breast cancer.
  • INPP4B represents a potential therapeutic target for cancers driven by aberrant PI3K/Akt signaling.

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