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FAM210B activates STAT1/IRF9/IFIT3 axis by upregulating IFN-α/β expression to impede the progression of lung

Xuejuan Gao1, Donglan Huang2, Ying Liu2

  • 1MOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou, China. tgaoxj@jnu.edu.cn.

Cell Death & Disease
|February 3, 2025
PubMed

Insights

Family with sequence similarity 210 member B (FAM210B) suppresses lung adenocarcinoma growth and metastasis by activating immune pathways. Down-regulation of FAM210B predicts poor survival in lung cancer patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Family with sequence similarity 210 member B (FAM210B) is a novel protein implicated in tumor development.
  • The specific role and mechanisms of FAM210B in lung adenocarcinoma (LUAD) progression are largely unknown.

Purpose of the Study:

  • To investigate the function of FAM210B in LUAD.
  • To elucidate the molecular mechanisms underlying FAM210B's role in LUAD progression.

Main Methods:

  • Analysis of public datasets for FAM210B expression and survival correlation.
  • In vitro and in vivo experimental models of LUAD.
  • RNA sequencing (RNA-seq) to identify regulated signaling pathways.
  • Investigation of the STAT1/IRF9/IFIT3 axis and type I interferon (IFN-α/β) production.
  • Identification of interacting partners, including TOM70 (Translocase of outer mitochondrial membrane 70).

Main Results:

  • FAM210B expression is down-regulated in LUAD cells, and low expression correlates with poor survival.
  • FAM210B inhibits LUAD cell proliferation and metastasis in vitro and in vivo.
  • FAM210B regulates innate immune signaling, specifically upregulating IFN-α/β production.
  • FAM210B activates the STAT1/IRF9/IFIT3 pathway, suppressing LUAD cell viability and migration.
  • TOM70 is identified as a functional partner of FAM210B in modulating IFN-α/β expression and LUAD phenotypes.

Conclusions:

  • FAM210B acts as a tumor suppressor in LUAD.
  • FAM210B inhibits LUAD progression by activating the IFN-α/β-mediated immune response via the STAT1/IRF9/IFIT3 axis.
  • FAM210B's interaction with TOM70 is crucial for its tumor-suppressive functions in LUAD.

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