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ORIGINAL ARTICLE
Year : 2018  |  Volume : 7  |  Issue : 1  |  Page : 143

miR-30a Inhibits Melanoma Tumor Metastasis by Targeting the E-cadherin and Zinc Finger E-box Binding Homeobox 2


1 Applied Physiology Research Center, Cardiovascular Research Institute, Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Correspondence Address:
Prof. Shaghayegh Haghjooy Javanmard
Applied Physiology Research Center, Cardiovascular Research Institute, Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/abr.abr_146_18

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Background: Epithelial–mesenchymal transition (EMT) is actively involved in tumor invasion. The main hallmark of EMT is downregulation of the adherens junction protein E-cadherin due to transcriptional repression. Candidate E-cadherin transcription repressors are members of ZEB family, ZEB2 belong to the ZEB family transcription factor that is pivotal for embryonic development and tumor progression. ZEB2 (zinc finger E-box binding homeobox 2) is most widely known as an inducer of EMT. Growing evidence have shown the involvement of microRNAs in cancer progression. In this study, we demonstrate that miR-30a is a potent suppressor of melanoma metastasis to the lung. Materials and Methods: In this study, miR-30a has been transfected into B16-F10 melanoma cells, and then cells were injected intravenously into C57BL/6 mice. Then, the mice were sacrificed and nodules in the lungs were enumerated. Results: Ectopic expression of miR-30a in melanoma cell line resulted in the suppression of pulmonary metastasis. We also found that transfected miR-30a into melanoma cells could increase E-cadherin and decrease ZEB2 expression. Conclusions: Our findings showed that increased expression of miR-30a in melanoma inhibited metastasis in vivo by targeting ZEB2 and E-cadherin.


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