Akt as a therapeutic target in cancer

Linda S Steelman1, Kristin M Stadelman, William H Chappell

  • 1Brody School of Medicine at East Carolina University, Department of Microbiology & Immunology, Greenville, NC 27858, USA.

Abstract

Insights

The phosphatidylinositol 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/v-akt murine thymoma viral oncogene homolog (Akt)/mammalian target of rapamycin (mTOR) pathway is frequently altered in cancers. Targeting this pathway may offer new, effective cancer therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • The PI3K/PTEN/Akt/mTOR pathway is crucial for transmitting growth signals from cell surface receptors.
  • Aberrant regulation of this pathway is implicated in cancer development.

Purpose of the Study:

  • To review how mutations lead to elevated PI3K/PTEN/Akt/mTOR pathway expression and malignant transformation.
  • To discuss the potential of targeting this pathway for cancer therapy.

Main Methods:

  • Literature search for studies on altered PI3K/PTEN/Akt/mTOR pathway expression in various cancers.
  • Included cancers: hematopoietic, melanoma, lung, pancreatic, endometrial, ovarian, breast, prostate, and hepatocellular.

Main Results:

  • The PI3K/PTEN/Akt/mTOR pathway is frequently dysregulated across numerous cancer types.
  • Evidence suggests targeting this pathway can suppress abnormal cancer cell growth.

Conclusions:

  • Aberrant PI3K/PTEN/Akt/mTOR pathway regulation is common in diverse cancers.
  • Small molecule inhibitors targeting this pathway hold promise for novel and effective anticancer treatments.

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