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SOCS3 transactivation by PPARγ prevents IL-17-driven cancer growth

Hélène Berger1, Frédérique Végran, Madijd Chikh

  • 1Institut National de la Santé et de la Recherche Medicale (INSERM), U866, France.

Cancer Research
|April 27, 2013
PubMed

Insights

Docosahexaenoic acid (DHA) activates PPARγ, leading to SOCS3 expression. This inhibits T-helper 17 (TH17) cell differentiation and reduces IL-17 production, thereby preventing cancer growth in mice.

Area of Science:

  • Molecular Biology
  • Immunology
  • Cancer Research

Background:

  • Peroxisome proliferator-activated receptor gamma (PPARγ) activation by docosahexaenoic acid (DHA) influences proinflammatory cytokine secretion.
  • The intracellular signaling pathways regulated by PPARγ are not fully understood.
  • Proinflammatory T-helper 17 (TH17) cells play a role in inflammatory conditions and cancer.

Purpose of the Study:

  • To identify novel intracellular signaling pathways regulated by PPARγ activation.
  • To investigate the role of PPARγ-mediated signaling in T-helper 17 cell differentiation and function.
  • To determine the impact of DHA-PPARγ signaling on cancer development and progression.

Main Methods:

  • Identification of SOCS3 as a transcriptional target of PPARγ through promoter binding assays.
  • Assessment of TH17 cell differentiation and interleukin-17 (IL-17) production in vitro and in vivo.
  • Evaluation of DHA's effect on tumor outgrowth and angiogenesis in mouse cancer models.

Main Results:

  • PPARγ directly binds to and transactivates the SOCS3 gene promoter.
  • DHA-activated PPARγ suppresses TH17 cell differentiation and IL-17 production.
  • DHA administration reduced tumor growth and angiogenesis in mouse models, dependent on IL-17 signaling.

Conclusions:

  • SOCS3 is a critical transcriptional target of PPARγ, mediating its anti-inflammatory effects.
  • The PPARγ-SOCS3 pathway inhibits TH17 cell differentiation, offering a novel mechanism to control IL-17-driven inflammation.
  • DHA-mediated inhibition of IL-17-dependent cancer growth highlights a potential therapeutic strategy.

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