4.8 Article

FAM49B, a novel regulator of mitochondrial function and integrity that suppresses tumor metastasis

期刊

ONCOGENE
卷 37, 期 6, 页码 697-709

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SPRINGERNATURE
DOI: 10.1038/onc.2017.358

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资金

  1. Associazione Italiana Ricerca sul Cancro (5 x mille) [12182, 15257, 15232]
  2. University of Turin-Progetti Ateneo-Compagnia di San Paolo (PC-METAIMMUN-OTHER)
  3. University of Turin-Progetti Ateneo-Compagnia di San Paolo (PANTHER)
  4. Italian Ministry of Health-Progetti Ricerca Finalizzata [RF-2013-02354892]
  5. Fondazione Ricerca Molinette Onlus
  6. Fondazione Nadia Valsecchi
  7. European Community FP7 Grant Cam-Pac [602783]
  8. FIMP, Ministero Salute [CUP_J33G13000210001]
  9. Fondazione Ursula e Giorgio Cytron, Torino

向作者/读者索取更多资源

Mitochondrial dysregulation plays a central role in cancers and drives reactive oxygen species (ROS)-dependent tumor progression. We investigated the pro-tumoral roles of mitochondrial dynamics and altered intracellular ROS levels in pancreatic ductal adenocarcinoma (PDAC). We identified 'family with sequence similarity 49 member B' (FAM49B) as a mitochondria-localized protein that regulates mitochondrial fission and cancer progression. Silencing FAM49B in PDAC cells resulted in increased fission and mitochondrial ROS generation, which enhanced PDAC cell proliferation and invasion. Notably, FAM49B expression levels in PDAC cells were downregulated by the tumor microenvironment. Overall, the results of this study show that FAM49B acts as a suppressor of cancer cell proliferation and invasion in PDAC by regulating tumor mitochondrial redox reactions and metabolism.

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