miR-195 is a key regulator of Raf1 in thyroid cancer

被引：41
作者：
Wang, Fangzheng [1 ,2 ]
Jiang, Chuner [3 ]
Sun, Quanquan [1 ,2 ]
Yan, Fenqin [1 ,2 ]
Wang, Lei [1 ,2 ]
Fu, Zhenfu [1 ,2 ]
Liu, Tongxin [1 ,2 ]
Hu, Fujun [1 ,2 ]
机构：
[1] Zhejiang Canc Hosp, Dept Radiat Oncol, Hangzhou 310022, Zhejiang, Peoples R China
[2] Zhejiang Canc Hosp, Zhejiang Key Lab Radiat Oncol, Hangzhou 310022, Zhejiang, Peoples R China
[3] Zhejiang Canc Hosp, Dept Breast Surg, Hangzhou 310022, Zhejiang, Peoples R China
来源：
ONCOTARGETS AND THERAPY | 2015年 / 8卷
关键词：
Raf1; microRNA; thyroid cancer; proliferation; HEPATOCELLULAR-CARCINOMA CELLS; CHRONIC LYMPHOCYTIC-LEUKEMIA; BREAST-CANCER; LUNG-CANCER; COLORECTAL-CANCER; PROSTATE-CANCER; DOWN-REGULATION; NSCLC CELLS; RT-PCR; MICRORNAS;
D O I：
10.2147/OTT.S90710
中图分类号：
Q81 [生物工程学（生物技术）]; Q93 [微生物学];
学科分类号：
071005 ; 0836 ; 090102 ; 100705 ;
摘要：
Proto-oncogene Raf1 serves as a part of the mitogen-activated protein kinases/extracellular signal-regulated kinase signal transduction pathway and regulates cell migration, apoptosis, and differentiation. Although a large number of studies have shown that Raf1 is overexpressed in various kinds of cancer, little is known about the association between Raf1 and miRNAs in thyroid carcinoma. This study proves that Raf1 is overexpressed in thyroid cancer, which has been confirmed by many other studies. Besides, we identify that Raf1 is a direct target of miR-15a/b, miR-16, and miR-195 by dual luciferase reporter assay. We also find that the expression of miR-195 is downregulated in 50 pairs of thyroid tumor tissues compared to the adjacent nontumor tissues, while there is no difference in the expression of miR-15a/b and miR-16 between the groups. Furthermore, exogenous overexpression of miR-195 significantly inhibits the protein expression of Raf1 and blocks the thyroid cancer cell proliferation. Our findings delineate a novel mechanism for the regulation of Raf1 in thyroid cancer, which may help to provide a new direction for the treatment of thyroid cancer.
引用
收藏
页码：3021 / 3028
页数：8
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