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[TNFα induced IL-8 production through p38 MAPK- NF-kB pathway in human hepatocellular carcinoma cells]

Yao-hui Wang1, Jing-lin Xia, Wei-min Wang

  • 1Liver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai 200032, China.

Zhonghua Gan Zang Bing Za Zhi = Zhonghua Ganzangbing Zazhi = Chinese Journal of Hepatology
|April 25, 2012
PubMed
Abstract

Insights

Tumor necrosis factor-alpha (TNF-α) increases interleukin-8 (IL-8) production in liver cancer cells. The p38 mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kB) pathways are key regulators of this process.

Area of Science:

  • Molecular biology
  • Cell signaling
  • Oncology

Context:

  • Hepatocellular carcinoma (HCC) is a significant global health concern.
  • Interleukin-8 (IL-8) is a pro-inflammatory cytokine implicated in cancer progression.
  • Tumor necrosis factor-alpha (TNF-α) is a key mediator in inflammation and immunity.

Purpose:

  • To elucidate the role of the p38 MAPK-NF-kB signaling pathway in TNF-α-induced IL-8 production.
  • To investigate the molecular mechanisms underlying IL-8 regulation in human HCC cells (MHCC-97H).

Summary:

  • TNF-α significantly upregulated IL-8 production in MHCC-97H cells in a time- and dose-dependent manner.
  • TNF-α stimulation led to increased phosphorylation of p38 MAPK and nuclear translocation of NF-kB p65.
  • Inhibition of p38 MAPK (using SB203580) reduced IL-8 production and partially inhibited NF-kB p65 nuclear translocation.

Impact:

  • This study identifies the p38 MAPK-NF-kB pathway as a critical regulator of IL-8 production in HCC.
  • Understanding this pathway offers potential therapeutic targets for managing HCC-associated inflammation and progression.

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