RT Journal Article SR Electronic T1 Bacterial SOS Genes mucAB/umuDC Promote Mouse Tumors by Activating Oncogenes Nedd9/Aurkb via a miR-145 Sponge JF Molecular Cancer Research JO Mol Cancer Res FD American Association for Cancer Research SP 1271 OP 1277 DO 10.1158/1541-7786.MCR-20-0137 VO 18 IS 9 A1 Tanooka, Hiroshi A1 Inoue, Ayako A1 Takahashi, Ryou-u A1 Tatsumi, Kouichi A1 Fujikawa, Kazuo A1 Nagao, Tetsuji A1 Ishiai, Masamichi A1 Chiwaki, Fumiko A1 Aoyagi, Kazuhiko A1 Sasaki, Hiroki A1 Ochiya, Takahiro YR 2020 UL http://mcr.aacrjournals.org/content/18/9/1271.abstract AB The mechanism of cancer induction involves an aberrant expression of oncogenes whose functions can be controlled by RNAi with miRNA. Even foreign bacterial RNA may interfere with the expression of oncogenes. Here we show that bacterial plasmid mucAB and its Escherichia coli genomic homolog umuDC, carrying homologies that match the mouse anti-miR-145, sequestered the miR-145 function in mouse BALB 3T3 cells in a tetracycline (Tet)-inducible manner, activated oncogene Nedd9 and its downstream Aurkb, and further enhanced microcolony formation and cellular transformation as well as the short fragments of the bacterial gene containing the anti-miR-145 sequence. Furthermore, mucAB transgenic mice showed a 1.7-fold elevated tumor incidence compared with wild-type mice after treatments with 3-methylcolanthrene. However, the mutation frequency in intestinal stem cells of the mucAB transgenic mice was unchanged after treatment with X-rays or ethyl-nitrosourea, indicating that the target of mucAB/umuDC is the promotion stage in carcinogenesis.Implications: Foreign bacterial genes can exert oncogenic activity via RNAi, if endogenously expressed.Visual Overview: http://mcr.aacrjournals.org/content/molcanres/18/9/1271/F1.large.jpg.