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KCTD15 deregulation is associated with alterations of the NF-κB signaling in both pathological and physiological

Giovanni Smaldone1, Luigi Coppola1, Katia Pane1

  • 1IRCCS SDN, Via E. Gianturco 113, 80143, Naples, Italy.

Scientific Reports
|September 15, 2021
PubMed

Insights

KCTD15 protein influences the NF-κB pathway, impacting conditions from leukemia to obesity. Its upregulation correlates with increased NF-κB signaling, offering new insights into diverse biological roles.

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Cancer Research

Background:

  • KCTD15, a member of the KCTD protein family, participates in critical biological processes including cancer, neural crest formation, and obesity.
  • Understanding KCTD15's diverse functions across various physiological and pathological states is crucial.

Purpose of the Study:

  • To investigate the role of KCTD15 in different physiological and pathological conditions.
  • To elucidate the relationship between KCTD15 and the NF-κB signaling pathway.

Main Methods:

  • Silencing KCTD15 in MLL-rearranged leukemia models.
  • Stimulating peripheral blood T cells and analyzing CD34 hematopoietic stem/progenitor cells.
  • Employing luciferase assays, proximity ligation, and immunoprecipitation experiments.

Main Results:

  • KCTD15 silencing attenuated the NF-κB pathway in leukemia models, downregulating pIKK-β and pIKB-α.
  • T cell activation and CD34+ cell activation upregulated KCTD15, pIKK-β, and pIKB-α.
  • Experiments confirmed the association between KCTD15 upregulation and enhanced NF-κB signaling, with KCTD15 upregulating IKK-β.

Conclusions:

  • KCTD15 plays a significant role in regulating the NF-κB pathway.
  • The upregulation of IKK-β by KCTD15 provides a novel mechanism for its function in diverse conditions.
  • KCTD15's involvement spans neuronal development, cancer, and metabolic disorders like obesity and diabetes.

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