American Association for Cancer Research
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Supplemental Figures 1-7 from Bacterial SOS Genes mucAB/umuDC Promote Mouse Tumors by Activating Oncogenes Nedd9/Aurkb via a miR-145 Sponge

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journal contribution
posted on 2023-04-03, 17:47 authored by Hiroshi Tanooka, Ayako Inoue, Ryou-u Takahashi, Kouichi Tatsumi, Kazuo Fujikawa, Tetsuji Nagao, Masamichi Ishiai, Fumiko Chiwaki, Kazuhiko Aoyagi, Hiroki Sasaki, Takahiro Ochiya

Supplementary Fig. S1. Nedd9 and Aurkb seed match sequences in mucAB and umuDC.

Supplementary Fig. S2. Selection of cells expressing Tet-repressor protein.

Supplementary Fig. S3. Microarray analysis of deregulated oncogenes.

Supplementary Fig. S4. Suppression of cellular transformation with anti-mucAB shRNA.

Supplementary Fig. S5. Confirmation of interaction of miR-145 with anti-miR-145.

Supplementary Fig. S6. Microcolony formation over time.

Supplementary Fig. S7. Comparison of tumor incidence rates between males and females, and between presence and absence of Zn.


Grants-in-aid for Cancer Research

Ministry of Health and Welfare, Japan

Japan Agency for Medical Research and Development



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. Foreign bacterial genes can exert oncogenic activity via RNAi, if endogenously expressed.

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