microRNA-625 inhibits tumorigenicity by suppressing proliferation, migration and invasion in malignant melanoma

// Wei Fang 1, 3, * , Yibin Fan 6, * , Zhenzong Fa 1, * , Jinhua Xu 3 , Hongyu Yu 4 , Pu Li 5 , Julin Gu 1, 2 1 Shanghai Key Laboratory of Molecular Medical Mycology, Department of Dermatology and Venereology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China 2 Department of Dermatology, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 201805 China 3 Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, China 4 Department of Pathology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China 5 Department of Pediatrics, Ruijin Hospital and Ruijin Hospital North, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200025, People’s Republic of China 6 Department of Dermatology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, 310014, China * These authors have contributed equally to this work Correspondence to: Pu Li, email: leerockygood@yahoo.com Julin Gu, email: wujgjl@126.com Keywords: malignant melanoma, miR-625, tumorigenesis, SOX2 Received: July 29, 2016      Accepted: December 12, 2016      Published: January 18, 2017 ABSTRACT Dysregulated microRNA (miR)-625 expression has been observed in several kinds of cancer. MicroRNAs are important factors in the development and progression of malignant melanoma, though the clinical significance and function of miR-625 in human malignant melanoma remain unclear. Levels of miR-625 expression were therefore determined in 36 pairs of malignant melanoma and adjacent non-tumor tissue using qPCR. The effects of miR-625 dysregulation on malignant melanoma cell proliferation, wound healing, migration and invasion in vitro and tumorigenicity in vivo were investigated using CCK-8, transwell assays, and a nude mouse subcutaneous tumor model. Bioinformatics analysis and luciferase reporter system were used to predict and confirm the target gene of miR-625. miR-625 levels were frequently decreased in malignant melanoma. Ectopic expression of miR-625 suppressed proliferation, wound healing, migration, and tumorgenicity in malignant melanoma. Moreover, miR-625 acted, at least in part, by suppressing potential target SOX2 . These results show that miR-625 is a tumor suppressor that inhibits the development and progression of malignant melanoma, which suggests miR-625 is potentially a new diagnostic marker and therapeutic target of malignant melanoma.