标题:Suppression of SIK1 by miR-141 in human ovarian cancer cell lines and tissues
作者:Chen, Jin-Long; Chen, Fang; Zhang, Ting-Ting; Liu, Nai-Fu
作者机构:[Chen, Jin-Long] Shandong Univ, Shandong Acad Med Sci, Shandong Canc Hosp, Univ Jinan Shandong Acad Med Sci,Sch Med & Life S, Jinan 250117, Shandong, 更多
通讯作者:Liu, NF
通讯作者地址:[Liu, NF]Shandong Univ, Shandong Acad Med Sci, Shandong Canc Hosp, 440 Jiyan Rd, Jinan 250117, Shandong, Peoples R China.
来源:INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
出版年:2016
卷:37
期:6
页码:1601-1610
DOI:10.3892/ijmm.2016.2553
关键词:ovarian cancer; salt-inducible kinase 1; miR-141
摘要:Epithelial ovarian cancer (EOC), the sixth most common cancer in women worldwide, is the most commonly fatal gynecologic malignancy in developed countries. One of the main reasons for this is that relatively little was known about the molecular events responsible for the development of this highly aggressive disease. In the present study, we demonstrated that salt-inducible kinase 1 (SIK1; which is also known as MSK/SIK/SNF1LK) was downregulated in ovarian cancer tissue samples. Using HEY ovarian cancer cells, we noted that SIK1 overexpression inhibited proliferation as well as cancer stem cell-associated traits. Silencing SIK1 promoted the proliferation of the EG ovarian cancer cell line. We performed an analysis of potential microRNAs (miRNAs or miRs) target sites using three commonly used prediction algorithms: miRanda, TargetScan and PicTar. All three algorithms predicted that miR-141 targets the 3UTR of SIK1. Subsequent experiments not only confirmed this prediction, but also showed that miR-141 was associated with the progression of this disease. Finally, we found that miR-141 promoted proliferation of EG cells, whereas silencing miR-141 restored SIK1 expression and inhibited the proliferation of the HEY cells. Elucidating the molecular mechanism of ovarian cancer not only enables us to further understand the pathogenesis and progression of the disease, but also provides new targets for effective therapies.
收录类别:SCOPUS;SCIE
WOS核心被引频次:2
Scopus被引频次:2
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84978903997&doi=10.3892%2fijmm.2016.2553&partnerID=40&md5=b594111273888db8c689c086a2c2c808
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