IR@PKUHSC  > 基础医学院  > 细胞生物学系
学科主题基础医学
MicroRNA 145 may play an important role in uveal melanoma cell growth by potentially targeting insulin receptor substrate-1
Li Yang1,2; Huang Qiming1,2; Shi Xuehui1,2; Jin Xiang1,2; Shen Li3,4; Xu Xiaolin1,2; Wei Wenbin1,2
关键词Uveal Melanoma Microrna Array Mir-145 Insulin Receptor Substrate-1
刊名CHINESE MEDICAL JOURNAL
2014-04-20
DOI10.3760/cma.j.issn.0366-6999.20133206
127期:8页:1410-1416
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Medicine, General & Internal
资助者National Natural Science Foundation of China ; Natural Sciences Fundation of Beijing, China ; National Natural Science Foundation of China ; Natural Sciences Fundation of Beijing, China
研究领域[WOS]General & Internal Medicine
关键词[WOS]EXPRESSION SIGNATURE ; BREAST-CANCER ; MIGRATION ; SUPPRESSES ; MIR-145 ; TUMORS ; OVEREXPRESSION ; PROLIFERATION ; METASTASIS ; INVASION
英文摘要

Background MicroRNAs (miRNAs) contribute to tumorigenesis by acting as either oncogenes or tumor suppressor genes. In this Study, we investigated the role of miR-145 in the pathogenesis of uveal melanoma.

Methods Expression profiles of miRNAs in uveal melanoma were performed using Agilent miRNA array. Quantitative real-time polymerase chain reaction was used to screen The expression levels of miR-145 in normal uveal tissue, uveal melanoma tissue, and uveal melanoma cell lines. Lenti-virus expression system was used to construct MUM-2B and OCM-1 cell lines with stable overexpression of miR-145. Cell proliferation, cell cycle, and cell apoptosis of these miR-145 overexpression cell lines were examined by MTT assay and flow cytometry respectively. The target genes of miR-145 were predicted by bioinformatics and confirmed using a luciferase reporter assay. The expression of insulin-like growth factor-1 receptor (IGF-1R), insulin receptor substrate-1 (IRS-1) proteins was determined by Western blotting analysis. IRS-1 was knocked down in OCM-1 cells. TUNEL, BrdU, and flow cytometry assay were performed in IRS-1 knocked down OCM-1 cell lines to analyze its function.

Results Forty-seven miRNAs were up regulated in uveal melanoma and 61 were down regulated. miR-145 expression was significantly lower in uveal melanoma sample and the cell lines were compared with normal uveal sample. Overexpression of miR-145 suppressed cell proliferation by blocking the G1 phase entering S phase in uveal melanoma cells, and promoted uveal melanoma cell apoptosis. IRS-1 was identified as a potential target of miR-145 by dual luciferase reporter assay. Knocking down of IRS-1 had similar effect as overexpression of miR-145.

Conclusion miR-145 might act as a tumor suppressor in uveal melanoma, and downregulation of the target IRS-1 might be a potential mechanism.

语种英语
所属项目编号81272981 ; 7112031
资助者National Natural Science Foundation of China ; Natural Sciences Fundation of Beijing, China ; National Natural Science Foundation of China ; Natural Sciences Fundation of Beijing, China
WOS记录号WOS:000335936700004
引用统计
被引频次:6[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/50753
专题基础医学院_细胞生物学系
作者单位1.Capital Med Univ, Beijing Tongren Hosp, Beijing Tongren Eye Ctr, Beijing 100730, Peoples R China
2.Beijing Key Lab Ophthalmol & Visual Sci, Beijing 100730, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Dept Cell Biol, Beijing 100191, Peoples R China
4.Peking Univ, Stem Cell Res Ctr, Beijing 100191, Peoples R China
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GB/T 7714
Li Yang,Huang Qiming,Shi Xuehui,et al. MicroRNA 145 may play an important role in uveal melanoma cell growth by potentially targeting insulin receptor substrate-1[J]. CHINESE MEDICAL JOURNAL,2014,127(8):1410-1416.
APA Li Yang.,Huang Qiming.,Shi Xuehui.,Jin Xiang.,Shen Li.,...&Wei Wenbin.(2014).MicroRNA 145 may play an important role in uveal melanoma cell growth by potentially targeting insulin receptor substrate-1.CHINESE MEDICAL JOURNAL,127(8),1410-1416.
MLA Li Yang,et al."MicroRNA 145 may play an important role in uveal melanoma cell growth by potentially targeting insulin receptor substrate-1".CHINESE MEDICAL JOURNAL 127.8(2014):1410-1416.
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