Mechanism and Application Prospects of NLRC3 Regulating cGAS-STING Pathway in Lung Cancer Immunotherapy

Int J Med Sci. 2024 Oct 7;21(13):2613-2622. doi: 10.7150/ijms.102328. eCollection 2024.

Abstract

NLRC3, a negative regulator, exhibits considerable potential in the realm of lung cancer immunotherapy by virtue of its profound impact on the immune response intensity, primarily through its regulatory effects on the cGAS-STING pathway. The inhibition of NLRC3 has been found to augment the activity of the aforementioned pathway, thereby enhancing the anti-tumor immune response. This comprehensive review endeavors to elucidate the molecular and genetic structures of NLRC3, its role within the immune system, and its interaction with the cGAS-STING pathway, with a particular emphasis on its potential applications in lung cancer immunotherapy. Existing research underscores NLRC3's capacity to mitigate excessive immune responses via the negative regulation of the cGAS-STING pathway, thus underscoring its significant regulatory role in lung cancer immunotherapy. The development of pharmaceutical interventions and gene therapy strategies targeting NLRC3 presents a promising avenue for the creation of novel therapeutic options for individuals afflicted with lung cancer. Nonetheless, the clinical application of these therapies is confronted with both technical and biological challenges. This review aims to provide a theoretical foundation for related research endeavors and delineate future research directions in this field.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Immunotherapy* / methods
  • Intercellular Signaling Peptides and Proteins
  • Intracellular Signaling Peptides and Proteins / genetics
  • Intracellular Signaling Peptides and Proteins / immunology
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Lung Neoplasms* / genetics
  • Lung Neoplasms* / immunology
  • Lung Neoplasms* / therapy
  • Membrane Proteins* / genetics
  • Membrane Proteins* / metabolism
  • Nucleotidyltransferases* / genetics
  • Nucleotidyltransferases* / metabolism
  • Signal Transduction* / immunology

Substances

  • Membrane Proteins
  • Nucleotidyltransferases
  • NLRC3 protein, human
  • STING1 protein, human
  • cGAS protein, human
  • Intracellular Signaling Peptides and Proteins
  • Intercellular Signaling Peptides and Proteins