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Power of PTEN/AKT: Molecular switch between tumor suppressors and oncogenes

Yingqiu Xie1, Sanzhar Naizabekov1, Zhanlin Chen2

  • 1Department of Biology, Nazarbayev University, School of Science and Technology, Astana 010000, Republic of Kazakhstan.

Oncology Letters
|June 28, 2016
PubMed

Insights

Tumor suppressors can become oncogenes and vice versa, with phosphatase and tensin homolog (PTEN) acting as a key switch. PTEN loss or AKT activation alters tumor suppressor and oncogene functions, impacting cancer pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Tumor suppressors can function as oncogenes and vice versa, a phenomenon with unclear underlying mechanisms.
  • Phosphatase and tensin homolog (PTEN) is implicated as a critical regulator in this functional switch.
  • PTEN influences cell death and proliferation via the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway.

Purpose of the Study:

  • To review cases of PTEN loss and/or AKT activation.
  • To analyze aberrant signaling pathways and identify novel drug targets for personalized cancer medicine.
  • To elucidate the mechanisms by which PTEN loss influences oncogene and tumor suppressor conversion.

Main Methods:

  • Literature review of studies focusing on PTEN loss and AKT activation.
  • Analysis of specific cases involving PTEN loss/AKT activation and their impact on tumor suppressor and oncogenic proteins.
  • Examination of molecular mechanisms driving the conversion between oncogene and tumor suppressor roles.

Main Results:

  • PTEN loss/AKT activation leads to MDM2-dependent p53 downregulation.
  • This alteration induces functional conversion between oncogene and tumor suppressor roles for proteins including EZH2, BCL7A, ARF2, p27, and BRCA1.
  • Multiple mechanisms contribute to these functional switches.

Conclusions:

  • PTEN loss and AKT activation are pivotal in switching the roles of key cancer-related proteins.
  • Understanding these genetic underpinnings reveals complex drug targets.
  • This knowledge provides a rationale for developing precision cancer therapies.
Keywords:
PTENmolecular switchoncogenetumor suppressor

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