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Updated: May 15, 2026

Quantification of Cytokine-Induced Cell Death in Human Colonic Organoids Using Live Fluorescence Microscopy
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Quantification of Cytokine-Induced Cell Death in Human Colonic Organoids Using Live Fluorescence Microscopy

Published on: August 2, 2024

IL-32γ enhances TNF-α-induced cell death in colon cancer

Eun-Seok Park1, Jae-Myung Yoo, Hwan-Soo Yoo

  • 1Division of Life Science, Department of Applied Biochemistry, College of Health and Biomedical Science, Konkuk University, Chungju, Korea.

Molecular Carcinogenesis
|December 21, 2012
PubMed

Insights

Interleukin-32 gamma (IL-32γ) combined with TNF-α significantly inhibits colon cancer cell and tumor growth. This cytokine combination activates apoptosis and key signaling pathways, offering a potential therapeutic strategy for colon cancer.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Interleukin-32 (IL-32) is a novel cytokine implicated in human colon cancer progression.
  • IL-32γ is a specific isoform of IL-32 with potential roles in cancer therapy.

Purpose of the Study:

  • To investigate the combined effects of IL-32γ and TNF-α on human colon cancer cell and tumor growth.
  • To elucidate the underlying molecular mechanisms, including apoptosis and signaling pathway activation.

Main Methods:

  • In vitro studies using human colon cancer cell lines (HCT116, SW620) with IL-32γ overexpression or siRNA knockdown.
  • In vivo studies using a xenograft mouse model with IL-32γ-transfected HCT116 cells.
  • Analysis of cell proliferation, apoptosis markers, and key signaling proteins (p38 MAPK, Bax, Bcl-2, caspases).
  • Measurement of serum cytokine levels (IL-10, IL-6).

Main Results:

  • IL-32γ and TNF-α synergistically inhibited colon cancer cell proliferation, DNA synthesis, and tumor growth in mice.
  • Overexpression of IL-32γ enhanced TNF-α-induced apoptosis by upregulating Bax, cleaved caspase-3/9, and downregulating Bcl-2 and IAPs.
  • IL-32γ overexpression potentiated TNF-α-mediated p38 MAPK activation.
  • In vivo, IL-32γ-expressing tumors showed increased apoptosis and altered serum cytokine profiles (increased IL-10, decreased IL-6).

Conclusions:

  • IL-32γ significantly potentiates TNF-α-induced anti-cancer effects in colon cancer.
  • The mechanism involves the activation of p38 MAPK and modulation of apoptotic pathways.
  • IL-32γ represents a promising therapeutic target for colon cancer treatment.
Keywords:
TNF-αcell deathcolon cancercytokineinterleukin-32γ

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