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Updated: Apr 14, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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IL-32α suppresses colorectal cancer development via TNFR1-mediated death signaling

Hyung-Mun Yun1, Kyung-Ran Park1, Eun-Cheol Kim1

  • 1Department of Maxillofacial Tissue Regeneration, School of Dentistry and Research Center for Tooth & Periodontal Regeneration (MRC), Kyung Hee University, Seoul 130-701, Republic of Korea.

Oncotarget
|April 25, 2015
PubMed

Insights

Interleukin-32 alpha (IL-32α) suppresses colon cancer by enhancing tumor cell death signaling. This finding suggests IL-32α could be a therapeutic target for inflammation-linked colorectal cancer.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Inflammation creates a microenvironment conducive to cancer development.
  • Interleukin-32 (IL-32) is implicated in human cancers associated with chronic inflammation.

Purpose of the Study:

  • To investigate the role of Interleukin-32 alpha (IL-32α) in inflammation-driven colorectal carcinogenesis.
  • To elucidate the mechanisms by which IL-32α influences colon cancer development.

Main Methods:

  • Generation of a transgenic mouse model expressing IL-32α (IL-32α-Tg).
  • Induction of colon cancer in mice using azoxymethane (AOM).
  • Analysis of tumor incidence, TNFR1 expression, apoptosis, reactive oxygen species (ROS) production, and JNK activation.

Main Results:

  • IL-32α transgenic mice exhibited decreased AOM-induced colon cancer incidence.
  • Expression of TNFR1 and TNFR1-mediated apoptosis were increased in IL-32α-Tg mice.
  • IL-32α elevated ROS production, leading to sustained JNK activation, and was found to be upregulated in human colon cancer patients alongside TNFR1.

Conclusions:

  • IL-32α suppresses colon cancer development.
  • This suppression is mediated by promoting TNFR1-dependent apoptosis signaling.
  • IL-32α may represent a novel therapeutic target for colorectal cancer prevention and treatment.
Keywords:
IL-32αRIP1TNFR1colon cancer

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