title: microRNA-625 inhibits tumorigenicity by suppressing proliferation, migration and invasion in malignant melanoma.
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.
authors.affiliation: Shanghai Key Laboratory of Molecular Medical Mycology, Department of Dermatology and Venereology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.|Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Fang
authors.affiliation: Department of Dermatology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, 310014, China.
authors.forename: Yibin
authors.initials: Y
authors.lastname: Fan
authors.affiliation: Shanghai Key Laboratory of Molecular Medical Mycology, Department of Dermatology and Venereology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.
authors.forename: Zhenzong
authors.initials: Z
authors.lastname: Fa
authors.affiliation: Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
authors.forename: Jinhua
authors.initials: J
authors.lastname: Xu
authors.affiliation: Department of Pathology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.
authors.forename: Hongyu
authors.initials: H
authors.lastname: Yu
authors.affiliation: Department of Pediatrics, Ruijin Hospital and Ruijin Hospital North, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200025, People's Republic of China.
authors.forename: Pu
authors.initials: P
authors.lastname: Li
authors.affiliation: Shanghai Key Laboratory of Molecular Medical Mycology, Department of Dermatology and Venereology, Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.|Department of Dermatology, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 201805 China.
authors.forename: Julin
authors.initials: J
authors.lastname: Gu
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D000818:Animals; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic; D057809:HEK293 Cells; D006801:Humans; D008297:Male; D008545:Melanoma / Q000235:genetics* / Q000473:pathology; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D035683:MicroRNAs / Q000235:genetics*; D009361:Neoplasm Invasiveness; D020133:Reverse Transcriptase Polymerase Chain Reaction; D055748:SOXB1 Transcription Factors / Q000235:genetics; D014183:Transplantation, Heterologous; D047368:Tumor Burden / Q000235:genetics
chemical_list: D020413:3' Untranslated Regions; C575476:MIRN625 microRNA, human; D035683:MicroRNAs; C527782:SOX2 protein, human; D055748:SOXB1 Transcription Factors
keywords: SOX2; malignant melanoma; miR-625; tumorigenesis