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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

IL-17 mediated inflammation promotes tumor growth and progression in the skin

Donggou He1, Hui Li, Nabiha Yusuf

  • 1Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.

Plos One
|February 24, 2012
PubMed

Insights

Interleukin-17 (IL-17) signaling promotes inflammation-driven skin tumor development. Blocking IL-17 or its receptor inhibits tumor progression and suggests therapeutic potential for IL-17 targeting in cancer prevention and treatment.

Area of Science:

  • Oncology
  • Immunology
  • Dermatology

Background:

  • Inflammation's role in tumor development is critical but not fully understood.
  • Interleukin-17 (IL-17) is linked to inflammation-driven cancers, yet its precise mechanisms remain unclear.

Purpose of the Study:

  • To investigate the role of IL-17 receptor-A (IL-17R) in chemical carcinogen-induced skin carcinogenesis.
  • To elucidate the mechanisms by which IL-17 signaling influences inflammation-associated tumor development.

Main Methods:

  • Utilized IL-17 receptor-A gene-deficient (IL-17R-/-) mice in a chemical carcinogen-induced cutaneous carcinogenesis model.
  • Analyzed immune cell infiltration (CD8+ T cells, CD11b+ myeloid cells, myeloid-derived suppressor cells) and inflammatory markers.
  • Administered IL-17 neutralization antibodies in tumor-bearing mice.

Main Results:

  • IL-17R-/- mice exhibited resistance to skin carcinogenesis, with reduced inflammation, hyperplasia, and pro-tumor molecule production.
  • IL-17R deficiency led to increased CD8+ T cell infiltration and decreased myeloid cell infiltration and myeloid-derived suppressor cell development.
  • Pre-existing inflammation enhanced tumor susceptibility via IL-17-producing T cells, an effect abrogated in IL-17R-/- mice.
  • Neutralizing IL-17 inhibited tumor progression in established skin tumors.

Conclusions:

  • IL-17-mediated inflammation is a key driver of inflammation-associated tumor promotion.
  • Targeting IL-17 signaling offers a promising strategy for preventing and treating inflammation-driven cancers.

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