Cancer Science · 2016 · 86 citations · 35 references
Life SciencesMolecular BiologyOncologyCarcinogenesisGene ExpressionMolecular OncologyCervical CancerEpithelial-mesenchymal TransitionEpithelial-to-mesenchymal TransitionMicrorna BiologyMicrorna-mediated RegulationTumor Suppressor GenesCervical Cancer ChemotherapyEpithelial-mesenchymal Transition In CancerEpithelial-mesenchymal Transition MarkersMatched Control GroupMicrorna Function In CancerMicrorna In CancerMicrorna Regulation In CancerMicrorna Regulation Of Emt
Acquisition of epithelial-mesenchymal transition (EMT) has recently been proposed as an important contributor of drug resistance in cervical cancer cells. However, the underlying mechanisms are still unclear. MicroRNAs play a crucial role in regulating EMT. The aim of this study was to explore the potential role of miR-25-3p in regulating EMT in cisplatin-resistant (CR) cervical cancer cells. To this end, we established stable CR cervical cancer cells, HeLa-CR and CaSki-CR, and investigated the function of miR-25-3p in regulating EMT. It is found that CR cervical cancer cells possessed more EMT characteristics and demonstrated higher migratory abilities and invasiveness. miR-25-3p downregulation was also seen in HeLa-CR and CaSki-CR cells. Of note, ectopic expression of miR-25-3p reversed the EMT phenotype and sensitized CR cells to cisplatin via targeting Sema4C. Furthermore, stable overexpression of miR-25-3p in HeLa-CR cells suppressed tumor growth in mice, downregulated Sema4C and Snail, and upregulated E-cadherin compared with the control group. These results suggest that miR-25-3p is an important regulator of cervical cancer EMT and chemoresistance. Thus, upregulation of miR-25-3p could be a novel approach to treat cervical cancers that are resistant to chemotherapy.
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Ahmedin Jemal, Freddie Bray, Jacques Ferlay et al. · CA A Cancer Journal for Clinicians · 2011 · 55K citations · Full text
Yiwei Li, Timothy VandenBoom, Dejuan Kong et al. · Cancer Research · 2009 · 658 citations · Full text
Medicine, Cancer Biology, Oncology +17