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miR‑106b‑5p promotes cell cycle progression of malignant melanoma by targeting PTEN
Author(s) -
Xu-Ε Chen,
Pu Chen,
Shanshan Chen,
Ting Ma,
Guang Shi,
Ya Zhou,
Ji Li,
Liang Sheng
Publication year - 2017
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2017.6099
Subject(s) - pten , cell cycle , cyclin d1 , pi3k/akt/mtor pathway , transfection , cancer research , cell growth , protein kinase b , biology , mapk/erk pathway , cell , microbiology and biotechnology , cell culture , signal transduction , genetics
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.

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