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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Loss of the PTEN tumor suppressor gene accelerates cancer progression and treatment resistance.
  • Currently, no targeted therapies are available for PTEN-deficient tumors.

Purpose of the Study:

  • To identify a druggable mechanism driving tumorigenesis in PTEN-deficient cancers.
  • To investigate the role of PI3Kβ phosphorylation in PTEN-loss-driven cancer.

Main Methods:

  • Utilized BioID interactome analysis to uncover protein interactions.
  • Developed a selective antibody against phosphorylated PI3Kβ (p-PI3KβY962).
  • Tested the efficacy of dasatinib, an SRC/EPHA2 inhibitor, in preclinical models.

Main Results:

  • Identified a phosphorylation-dependent interaction between PI3Kβ and EPHA2, driven by p-PI3KβY962, in PTEN-null cells.
  • PTEN normally dephosphorylates p-PI3KβY962; its loss leads to enhanced p-PI3KβY962 formation.
  • Targeting p-PI3KβY962 suppressed tumor growth in PTEN-null models, and dasatinib showed efficacy in these models.

Conclusions:

  • Established p-PI3KβY962 as a critical druggable target and biomarker in PTEN-deficient cancers.
  • Demonstrated that targeting p-PI3KβY962 offers a novel therapeutic strategy beyond conventional PI3K inhibition.
  • SRC/EPHA2 inhibitors like dasatinib show promise for treating PTEN-null tumors.