{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T02:11:40Z","timestamp":1791079900650,"version":"4.1.0"},"reference-count":19,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2007,6,30]],"date-time":"2007-06-30T00:00:00Z","timestamp":1183161600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:p>The c13orf25\/miR\u201017 cluster, which is responsible for 13q31\u2010q32 amplification in malignant lymphoma, contains the microRNA\u201017\u201018\u201019\u201020\u201092 polycistron. A previous study demonstrated that this polycistron could modulate tumor formation following transplantation of microRNA 17\u201019b into Eu\u2010myc mice. Another study reported that Myc can upregulate the miR\u201017 cluster by binding directly upstream of the miR\u201017 locus. These findings suggest that Myc and the miR\u201017 cluster synergistically contribute to cancer development. In the study presented here, we observed recurrent 13q31\u201032 amplification in <jats:italic>MYC<\/jats:italic>\u2010rearranged lymphomas (11 of 47 cases). Quantitative real\u2010time polymerase chain reaction analysis of c13orf25 for <jats:italic>MYC<\/jats:italic>\u2010rearranged lymphomas demonstrated that cases with 13q31\u201032 amplification showed significantly higher expression of c13orf25 than cases without such amplification, although cases without 13q31\u201032 amplification still showed slight upregulation of c13orf25. To investigate the relationship between Myc and the miR\u201017 polycistron in tumorigenesis, we engineered rat fibroblasts (Rat\u20101) that constitutively express the miR\u201017 polycistron (miR), Myc, or both miR and Myc. The highest level of miR expression was detected in Rat\u20101 transfected with both miR and Myc, whereas Myc transfectant cells alone also showed slight upregulation of miR. Furthermore, we demonstrated that nude mice injected with Rat\u20101 transfected with both miR and Myc presented more accelerated tumor growth than those injected with Myc transfectant cells. These results suggest that miR is stably upregulated in the presence of constitutive expression of Myc, and that the deregulation of miR and Myc synergistically contribute to aggressive cancer development, probably by repressing tumor suppressor genes. 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