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Interleukin (IL)-24: Reconfiguring the Tumor Microenvironment for Eliciting Antitumor Response

Rajagopal Ramesh1,2,3, Rebaz Ahmed4,5, Anupama Munshi6,7

  • 1Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. rajagopal-ramesh@ouhsc.edu.

Advances in Experimental Medicine and Biology
|February 9, 2021
PubMed

Insights

Interleukin-24 (IL-24) shows promise as a cancer therapy by suppressing tumors. Further research is needed to explore its effects on the tumor microenvironment and immune response for enhanced cancer treatment strategies.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Interleukin-24 (IL-24) is a cytokine within the IL-10 family.
  • IL-24 exhibits dual functionality as a tumor suppressor and a cytokine.
  • IL-24-based cancer therapy is being developed for various human cancers.

Purpose of the Study:

  • To review the biological and functional characteristics of IL-24.
  • To summarize the therapeutic benefits of IL-24-based cancer treatments.
  • To highlight the underinvestigated role of IL-24 in modulating the tumor microenvironment and immune response.

Main Methods:

  • Literature review of existing studies on IL-24.
  • Analysis of IL-24's properties and therapeutic applications.
  • Synthesis of current knowledge on IL-24's impact on cancer.

Main Results:

  • IL-24 possesses significant tumor-suppressive capabilities.
  • Current research predominantly focuses on IL-24's direct tumor cell-killing effects.
  • The influence of IL-24 on the tumor microenvironment and immune modulation remains largely unexplored.

Conclusions:

  • IL-24 is a promising agent for cancer therapy.
  • Understanding IL-24's broader effects is crucial for optimizing its therapeutic potential.
  • Further investigation into IL-24's immunomodulatory and microenvironment-altering functions is warranted.

Keywords:
AngiogenesisApoptosisCancerCancer stem cellsCytokinesGlycosylationIL-10IL-19IL-20 receptorIL-22 receptorIL-24ImmunityMetastasisPhosphorylationPost-translational modificationUbiquitinationmda-7

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