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Ninjurin 2 Modulates Tumorigenesis, Inflammation, and Metabolism via Pyroptosis

Jin Zhang1, Xiangmudong Kong1, Hee Jung Yang1

  • 1Comparative Oncology Laboratory, University of California, Davis, Davis, California.

The American Journal of Pathology
|February 7, 2024
PubMed

Insights

Nerve injury-induced protein 2 (NINJ2) deficiency causes metabolic defects, inflammation, and tumors in mice. Loss of NINJ2 promotes pyroptosis, a cell death process linked to cancer and inflammation.

Area of Science:

  • Molecular Biology
  • Immunology
  • Metabolomics

Background:

  • Nerve injury-induced protein 2 (NINJ2) is an adhesion molecule primarily studied for its role in nerve regeneration.
  • The broader functions of NINJ2 in cellular processes beyond nerve repair remain largely unexplored.

Purpose of the Study:

  • To investigate the physiological roles of NINJ2 in vivo.
  • To elucidate the molecular mechanisms underlying NINJ2's function in metabolism, inflammation, and disease.

Main Methods:

  • Generation and characterization of Ninj2-deficient mice.
  • Comprehensive carbohydrate and lipid metabolic analyses (metabolomics).
  • Investigation of NINJ2's role in pyroptosis and inflammasome activation.

Main Results:

  • Ninj2-deficient mice exhibited reduced lifespan, spontaneous tumors, systemic inflammation, and metabolic dysfunction.
  • Metabolic analyses revealed defects in monosaccharide metabolism and altered lipid profiles (triglycerides, phospholipids, ceramides).
  • Loss of NINJ2 enhanced pyroptosis by activating the NLRP3 inflammasome.

Conclusions:

  • NINJ2 plays a critical role in maintaining metabolic homeostasis and suppressing spontaneous tumorigenesis and inflammation.
  • NINJ2 regulates pyroptosis, a programmed cell death pathway implicated in cancer, inflammation, and metabolic disorders.
  • These findings highlight NINJ2 as a potential therapeutic target for diseases involving aberrant pyroptosis, inflammation, and metabolic dysregulation.

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