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Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
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The role of RICTOR amplification in targeted therapy and drug resistance

Deze Zhao1, Man Jiang1, Xiaochun Zhang1

  • 1Department of Medical Oncology, The Affiliated Hospital of Qingdao University, Qingdao University, 16 Jiangsu Road, Qingdao, 266005, China.

Molecular Medicine (Cambridge, Mass.)
|February 12, 2020
PubMed

Insights

Targeting RICTOR, a key part of the PI3K-AKT pathway, may overcome resistance to tyrosine kinase inhibitors (TKIs) by blocking receptor tyrosine kinase (RTK) co-activation in cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Tyrosine kinase inhibitors (TKIs) have advanced cancer treatment, but receptor tyrosine kinase (RTK) co-activation can lead to resistance.
  • Understanding RTK co-activation networks is crucial for improving targeted cancer therapies.

Purpose of the Study:

  • To explore the role of RICTOR in tumor biology and its potential as a therapeutic target.
  • To discuss targeting RICTOR to overcome TKI resistance mediated by RTK co-activation.

Main Methods:

  • Review of current literature on RICTOR, PI3K-AKT-mTOR pathway, and RTK co-activation.
  • Analysis of RICTOR's biological functions in cancer phenotypes and treatment response.

Main Results:

  • RICTOR amplification is linked to poor clinical outcomes and TKI resistance.
  • RICTOR is a key effector in the PI3K-AKT pathway, downstream of RTKs.

Conclusions:

  • Targeting RICTOR presents a promising strategy to inhibit RTK co-activation.
  • RICTOR-targeted therapy could serve as a complementary approach to enhance TKI efficacy in cancer treatment.
Keywords:
Drug resistanceRICTORTKIsmTORC2

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