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Bacterial SOS Genes mucAB/umuDC Promote Mouse Tumors by Activating Oncogenes Nedd9/Aurkb via a miR-145 Sponge

Hiroshi Tanooka1,2,3, Ayako Inoue4, Ryou-U Takahashi4

  • 1Division of Molecular and Cellular Medicine, National Cancer Center Research Institute, Tokyo, Japan. tanooka-h@wind.ocn.ne.jp.

Molecular Cancer Research : MCR
|June 10, 2020
PubMed

Insights

Foreign bacterial genes, like mucAB, can promote cancer by interfering with microRNA (miRNA) regulation of oncogenes. This suggests bacterial RNA

Area of Science:

  • Molecular Biology
  • Oncology
  • Microbiology

Background:

  • Cancer induction involves oncogene dysregulation, potentially influenced by RNA interference (RNAi) via microRNA (miRNA).
  • Foreign bacterial RNA may also impact oncogene expression, contributing to carcinogenesis.

Purpose of the Study:

  • To investigate if bacterial genes mucAB and umuDC can influence oncogene expression and cellular transformation through RNAi mechanisms.
  • To determine the role of bacterial genes in cancer promotion and tumor incidence in vivo.

Main Methods:

  • Utilized mouse BALB 3T3 cells and mucAB transgenic mice.
  • Employed tetracycline-inducible systems to control bacterial gene expression.
  • Assessed oncogene activation (Nedd9, Aurkb), cellular transformation, tumor incidence, and mutation frequencies.

Main Results:

  • Bacterial mucAB/umuDC sequestered miR-145, activated oncogenes Nedd9 and Aurkb, and enhanced cellular transformation in mouse cells.
  • MucAB transgenic mice exhibited a 1.7-fold increase in tumor incidence after chemical carcinogen treatment.
  • No change in mutation frequency in intestinal stem cells indicated that bacterial genes target the promotion stage of carcinogenesis.

Conclusions:

  • Endogenously expressed foreign bacterial genes can possess oncogenic activity by interfering with host RNAi pathways.
  • Bacterial genes mucAB/umuDC promote cancer development, specifically at the stage of tumor promotion, not initiation.
  • This study highlights a novel mechanism of bacterial-mediated oncogenesis via RNA interference.

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