title: miR-425 inhibits melanoma metastasis through repression of PI3K-Akt pathway by targeting IGF-1.
abstract: miR-425 is a potential tumor suppressor in cancer, but its role in melanoma is still unknown. We aim to investigate miR-425 expression in melanoma tissues and cell lines. Next, cell proliferation, cell cycle, apoptosis and metastasis will be studied using lentivirus-mediated gain-of-function studies. The predicted results are stable miR-425 inhibits cell proliferation and metastasis and induced cell apoptosis. It is predicted that IGF-1 is a potential target gene of miR-495 by bioinformatics analysis. Then luciferase assay analysis identifies IGF-1 as a new direct target gene of miR-425 and miR-425 inhibits melanoma cancer progression via IGF-1. Collectively, our findings suggested that miR-425 may function as a tumor suppressor in melanoma by targeting IGF-1.
authors.affiliation: Department of Plastic Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
authors.forename: Pei
authors.initials: P
authors.lastname: Liu
authors.affiliation: Department of General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
authors.forename: Yaotian
authors.initials: Y
authors.lastname: Hu
authors.affiliation: Department of Plastic Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Ma
authors.affiliation: Department of Plastic Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
authors.forename: Min
authors.initials: M
authors.lastname: Du
authors.affiliation: Department of Plastic Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Xia
authors.affiliation: Department of Plastic Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China. Electronic address: hu_zhensheng@126.com.
authors.forename: Zhensheng
authors.initials: Z
authors.lastname: Hu
mesh_terms: D020413:3' Untranslated Regions; D017209:Apoptosis; D001665:Binding Sites; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism*; D008545:Melanoma / Q000201:enzymology* / Q000235:genetics* / Q000556:secondary; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D034622:RNA Interference; D015398:Signal Transduction; D012878:Skin Neoplasms / Q000201:enzymology* / Q000235:genetics* / Q000473:pathology; D013997:Time Factors; D014162:Transfection
chemical_list: D020413:3' Untranslated Regions; C583557:IGF1 protein, human; C555677:MIRN425 microRNA, human; D035683:MicroRNAs; D007334:Insulin-Like Growth Factor I; D058539:Phosphatidylinositol 3-Kinase; D051057:Proto-Oncogene Proteins c-akt
keywords: IGF-1; Melanoma; Metastasis; miR-425