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PTEN: Regulation, Signalling and Targeting in Cancer.

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Correction: Kotelevets, L.; Chastre, E. Extracellular Vesicles in Colorectal Cancer: From Tumor Growth and Metastasis to Biomarkers and Nanomedications. <i>Cancers</i> 2023, <i>15</i>, 1107.

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Related Experiment Video

Updated: Jan 31, 2026

Orthotopic Mouse Model of Colorectal Cancer
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Targeting PTEN in Colorectal Cancers.

Larissa Kotelevets1,2, Mark G H Scott3,4, Eric Chastre5,6

  • 1Inserm, UMR S 938, Cancer Biology and Therapeutics, Centre de Recherche Saint-Antoine, Paris, France.

Advances in Experimental Medicine and Biology
|January 10, 2019
PubMed
Summary

Phosphatase and tensin homolog (PTEN) is a crucial tumor suppressor. Restoring PTEN function in colon cancer cells offers a promising strategy to inhibit tumor growth and enhance therapeutic efficacy.

Keywords:
AKT signalingDNA repairMolecular scaffoldsPhosphataseTumor suppressor

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Phosphatase and tensin homolog (PTEN) is a key tumor suppressor gene frequently altered in human cancers.
  • PTEN regulates critical cellular processes including proliferation, apoptosis, and cell signaling, notably by dephosphorylating phosphoinositides and counteracting the Akt pathway.
  • While PTEN mutations are less common in colorectal cancers, downregulation and functional inactivation through posttranslational modifications or mislocalization are prevalent.

Purpose of the Study:

  • To review the regulatory mechanisms of PTEN expression, activity, and function in the context of cancer.
  • To explore strategies for pharmacologically restoring wild-type PTEN function in colon cancer cells.
  • To discuss small molecules targeting PTEN regulators and alternative methods to modulate PTEN activity.

Main Methods:

  • Literature review of PTEN regulation and function in cancer.
  • Analysis of PTEN's role in colorectal cancer, including genetic alterations and functional inactivation.
  • Examination of therapeutic strategies aimed at restoring PTEN activity.

Main Results:

  • PTEN inactivation in colorectal cancer occurs through downregulation, posttranslational modifications, and mislocalization, in addition to mutations.
  • Restoring PTEN function can inhibit colon cancer cell growth and induce apoptosis.
  • Small molecules and alternative strategies show potential for modulating PTEN activity and conformation.

Conclusions:

  • Pharmacological restoration of PTEN function is a viable therapeutic strategy for colon cancer.
  • Targeting PTEN regulators and modulating its activity could overcome PTEN inactivation in tumors.
  • A personalized approach to PTEN restoration may be beneficial for colon cancer treatment.