Department of Oncology, Zhongnan Hospital, Wuhan University, Wuhan, People's Republic of China.
PLoS One. 2012;7(12):e52310. doi: 10.1371/journal.pone.0052310. Epub 2012 Dec 20.
The epithelial-mesenchymal transition (EMT) induced by EGF promotes cervical cancer progression; however, the mechanisms underlying the EGF-induced EMT remain unclear. In this study, we reported that miR155 overexpression suppressed EGF-induced EMT, decreased migration/invasion capacities, inhibited cell proliferation and increased the chemo-sensitivity to DDP in human Caski cervical cancer cells. Further, the overexpression of miR155 increased TP53 expression but reduced SMAD2, and CCND1 expression levels. These data suggest that miR155 negatively regulates EGF-induced EMT. We conclude that miR155 does not act as an oncogene but as a tumour suppressor in Caski cells.
表皮间质转化（EMT）由 EGF 诱导，促进宫颈癌的进展；然而，EGF 诱导的 EMT 的机制尚不清楚。在这项研究中，我们报道 miR155 的过表达抑制了 EGF 诱导的 EMT，降低了迁移/侵袭能力，抑制了细胞增殖，并增加了人 Caski 宫颈癌细胞对 DDP 的化疗敏感性。此外，miR155 的过表达增加了 TP53 的表达，而降低了 SMAD2 和 CCND1 的表达水平。这些数据表明 miR155 负调控 EGF 诱导的 EMT。我们得出结论，miR155 在 Caski 细胞中不作为癌基因，而是作为肿瘤抑制因子发挥作用。
