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The tumor suppressor CYLD interacts with TRIP and regulates negatively nuclear factor kappaB activation by tumor

Alexandre Regamey1, Daniel Hohl, Jia Wei Liu

  • 1Department of Dermatology, CHUV, Lausanne, Switzerland.

The Journal of Experimental Medicine
|December 17, 2003
PubMed

Insights

CYLD protein, a tumor suppressor, inhibits NF-kappaB activation. This deubiquitinating activity, crucial for cylindroma tumor growth, involves interaction with TRIP.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cylindromas are benign skin tumors linked to CYLD gene mutations.
  • CYLD acts as a tumor suppressor, with its protein product containing a deubiquitinating domain.

Purpose of the Study:

  • To investigate the function of the CYLD protein.
  • To elucidate the molecular mechanisms underlying CYLD's tumor suppressor activity.

Main Methods:

  • Yeast two-hybrid screening to identify CYLD interactors.
  • Far Western analysis and co-immunoprecipitation to confirm protein interactions.
  • Investigation of NF-kappaB activation in HeLa cells.

Main Results:

  • Identified TRIP (TRAF-interacting protein) as a CYLD interactor.
  • Demonstrated that CYLD down-regulates NF-kappaB activation by TNF-alpha.
  • Showed CYLD's inhibitory effect depends on its central domain, TRIP interaction, and deubiquitinating activity.

Conclusions:

  • CYLD protein regulates NF-kappaB signaling pathway.
  • Constitutive NF-kappaB activation due to CYLD dysfunction may drive cylindroma hyperproliferation and tumor growth.

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