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Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
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PI3K/Akt/mTOR Signaling Pathway as a Target for Colorectal Cancer Treatment

Premila D Leiphrakpam1,2, Chandrakanth Are1,2

  • 1Graduate Medical Education, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA.

International Journal of Molecular Sciences
|March 28, 2024
PubMed

Insights

Targeted therapies have advanced colorectal cancer (CRC) treatment, but resistance necessitates understanding molecular pathways like PI3K/Akt/mTOR. This review explores PI3K/Akt/mTOR

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Pathway-specific targeted therapy has transformed colorectal cancer (CRC) treatment.
  • Tumor heterogeneity in CRC often leads to treatment resistance.
  • The phosphatidylinositol 3-kinase/protein kinase B/mammalian target of the rapamycin (PI3K/Akt/mTOR) pathway is frequently altered in CRC.

Purpose of the Study:

  • To review the role of the PI3K/Akt/mTOR signaling pathway in CRC.
  • To discuss current PI3K/Akt/mTOR-targeted agents for CRC treatment.
  • To highlight limitations and future directions in targeting this pathway for CRC.

Main Methods:

  • Literature review of studies on PI3K/Akt/mTOR signaling in CRC.
  • Analysis of clinical trial data for PI3K/Akt/mTOR inhibitors in CRC.
  • Synthesis of information on CRC molecular mechanisms and targeted therapies.

Main Results:

  • Aberrant PI3K/Akt/mTOR activation drives CRC initiation, progression, and metastasis.
  • This pathway is critical for the development of drug resistance in CRC.
  • Several PI3K/Akt/mTOR-targeted agents are in clinical trials for CRC.

Conclusions:

  • Understanding PI3K/Akt/mTOR signaling is crucial for overcoming CRC treatment resistance.
  • Targeting the PI3K/Akt/mTOR pathway offers potential for novel CRC therapies.
  • Further research is needed to optimize PI3K/Akt/mTOR-targeted agents and combination strategies for CRC.
Keywords:
AktPI3Kapoptosiscell survivalcolorectal cancerinhibitorsmTORtargeted therapy

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