Abstract
<div>Abstract<p>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 <i>mucAB</i> and its <i>Escherichia coli</i> genomic homolog <i>umuDC,</i> 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 <i>Nedd9</i> and its downstream <i>Aurkb,</i> 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, <i>mucAB</i> 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 <i>mucAB</i> transgenic mice was unchanged after treatment with X-rays or ethyl-nitrosourea, indicating that the target of <i>mucAB/umuDC</i> is the promotion stage in carcinogenesis.</p>Implications:<p>Foreign bacterial genes can exert oncogenic activity via RNAi, if endogenously expressed.</p>Visual Overview:<p><a href="http://mcr.aacrjournals.org/content/molcanres/18/9/1271/F1.large.jpg" target="_blank">http://mcr.aacrjournals.org/content/molcanres/18/9/1271/F1.large.jpg</a>.</p></div>
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