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Updated: Aug 5, 2026

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Published on: April 18, 2025

NLRC3 suppresses hepatocarcinogenesis by disrupting the HSP90-mediated TRAF6/MYC signalling activation

Shishun Huang1, Chen Zheng2, Zheng Zhang3

  • 1School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, 325035, China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|August 3, 2026
PubMed

Insights

NLRC3, a negative regulator of inflammation, suppresses liver cancer (HCC) by inhibiting TRAF6/MYC signaling. Its loss promotes HCC via a TRAF6-MYC feedback loop, suggesting HSP90 as a therapeutic target.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • NLRC3 negatively regulates inflammatory pathways and is linked to diseases.
  • Its role in hepatocellular carcinoma (HCC) pathogenesis is not well understood.

Purpose of the Study:

  • To elucidate the function and mechanism of NLRC3 in HCC development.
  • To investigate the association between NLRC3 expression and HCC prognosis.

Main Methods:

  • Analysis of NLRC3 expression in HCC tissues.
  • Assessment of hepatocarcinogenesis in NLRC3-deficient mice.
  • Investigation of the TRAF6/MYC/NF-κB signaling cascade.
  • Examination of NLRC3-HSP90 interactions and protein ubiquitination.

Main Results:

  • NLRC3 expression is downregulated in HCC and correlates with poor prognosis.
  • NLRC3 deficiency enhances susceptibility to chemically induced hepatocarcinogenesis.
  • NLRC3 suppresses HCC by inhibiting the TRAF6/MYC/NF-κB pathway.
  • NLRC3-HSP90 interaction disrupts TRAF6/MYC stabilization, preventing a positive feedback loop.

Conclusions:

  • NLRC3 acts as a tumor suppressor in HCC.
  • A novel NLRC3-MYC signaling axis is identified.
  • HSP90 inhibition is a potential therapeutic strategy for NLRC3-deficient HCC.
Keywords:
HSP90Hepatocellular carcinomaMYCNLRC3TRAF6

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