miR-106b-5p promotes cell cycle progression of malignant melanoma by targeting PTEN

• Published in: Oncology reports Vol. 39; no. 1; pp. 331 - 337
• Main Authors: Chen, Xu-E, Chen, Pu, Chen, Shan-Shan, Ma, Ting, Shi, Guang, Zhou, Ya, Li, Ji, Sheng, Liang
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.01.2018; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: 5' Untranslated Regions; Akt/ERK pathway; Care and treatment; Cell Cycle; Cell growth; Cell Line, Tumor; Cell Proliferation; Cyclin-dependent kinases; Development and progression; Disease Progression; Gene expression; Gene Expression Regulation, Neoplastic; Genetic aspects; Health aspects; Humans; Kinases; malignant melanoma; MAP Kinase Signaling System; Melanoma; Melanoma - genetics; MicroRNA; MicroRNAs - genetics; miR-106b-5p; PTEN; PTEN Phosphohydrolase - genetics; Skin cancer; Up-Regulation; United States > US; China
• ISSN: 1021-335X; 1791-2431; 1791-2431
• DOI: 10.3892/or.2017.6099

This study investigated how miR-106b-5p/PTEN signaling affects the cell cycle of malignant melanoma (MM) cells. miR-106b-5p mRNA was identified with qRT-PCR. Through transient transfection, miR-106b-5p or PTEN was upregulated and downregulated in MM cells. With such transfected cells, MTT assay, colony formation assay and flow cytometry were carried out to investigate the role of miR-106b-5p in cell cycle progression after the transfected cells were treated with reverse-regulation of miR-106b-5p or PTEN. Western blot analysis was used to quantify all proteins, and a luciferase reporter assay was carried out to validate miR-106b-5p targeting PTEN. miR-106b-5p mRNA was overexpressed in MM tissues and cell lines. MM cells with upregulated miR-106b-5p presented faster growth and shorter cell cycles, while those with knockdown of miR-106b-5p presented the opposite trend. PTEN was subject to post-transcriptional regulation of miR-106b-5p. Based on such a finding, further exploration was carried out to investigate the interaction between cyclin D1 and P27Kip1, with the finding that miR-106b-5p can stimulate cyclin D1 and suppress P27Kip1 via the Akt/ERK pathway. The results of this study suggest that miR-106b-5p may be a promoter in MM progression, possibly by targeting PTEN and thus regulating the downstream cell-cycle-related proteins and Akt/ERK pathway.