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

被引:19
|
作者
Chen, Xu-E [1 ]
Chen, Pu [2 ]
Chen, Shan-Shan [1 ]
Ma, Ting [1 ]
Shi, Guang [1 ]
Zhou, Ya [1 ]
Li, Ji [1 ]
Sheng, Liang [1 ]
机构
[1] Guizhou Prov Peoples Hosp, Dept Dermatol, 83 East Zhongshan Rd, Guiyang 550002, Guizhou, Peoples R China
[2] Guizhou Prov Hosp Tradit Chinese Med, Dept Informat, Guiyang 550001, Guizhou, Peoples R China
关键词
malignant melanoma; miR-106b-5p; PTEN; microRNA; cell cycle; Akt/ERK pathway; TUMOR-SUPPRESSOR GENE; DOWN-REGULATION; BREAST-CANCER; EXPRESSION; MICRORNAS; PROLIFERATION; ASSOCIATION; DOWNSTREAM; CLUSTER; GROWTH;
D O I
10.3892/or.2017.6099
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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 P27(Kip1), with the finding that miR-106b-5p can stimulate cyclin D1 and suppress P27(Kip1) 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.
引用
收藏
页码:331 / 337
页数:7
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