Latest studies have shown that deregulated pseudogene transcripts contribute to cancer working as competing endogenous RNAs. Our research group has recently demonstrated that the overexpression of two HMGA1 pseudogenes, HMGA1P6 and HMGA1P7, has a critical role in cancer progression. These pseudogenes work sustaining the expression of HMGA1 and other cancer-related genes. We generated a mouse model overexpressing HMGA1P6 to better study the HMGA1-pseudogene function in a more physiological context. Here, we show the proliferation rate and the susceptibility to senescence of mouse embryonic fibroblasts obtained from HMGA1P6-overexpressing mice to better characterize the HMGA1-pseudogene function. Indeed, our study reports that mouse embryonic fibroblasts (MEFs) derived from HMGA1P6 mice express higher HMGA1 mRNA and protein levels. Moreover, these cells grow faster and senesce later than wild-type sustaining the oncogenic role of ceRNA crosstalk mediated by HMGA1Ps.

最新研究表明，伪基因转录物的失控促进了作为竞争性内源RNA的癌症的工作。我们的研究小组最近证明，两个HMGA1假基因HMGA1P6和HMGA1P7的过表达在癌症进展中起关键作用。这些假基因可维持HMGA1和其他癌症相关基因的表达。我们生成的小鼠模型中过表达HMGA1P6更好地研究HMGA1更生理方面-pseudogene功能。在这里，我们显示了从HMGA1P6获得的小鼠胚胎成纤维细胞的增殖率和衰老敏感性。-过表达的小鼠可以更好地表征HMGA1-假基因的功能。实际上，我们的研究报告称，源自HMGA1P6小鼠的小鼠胚胎成纤维细胞（MEF）表达更高的HMGA1 mRNA和蛋白水平。而且，这些细胞比野生型生长更快，衰老更晚，从而维持了由HMGA1P介导的ceRNA串扰的致癌作用。