Expression patterns of miR-221 and its target Caspase-3 in different cancer cell lines
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  • 作者:Sercan Ergun ; Kaifee Arman ; Ebru Temiz ; ?brahim Bozgeyik…
  • 关键词:MiR ; 221 ; Caspase ; 3 ; Apoptosis ; Cancer cell line
  • 刊名:Molecular Biology Reports
  • 出版年:2014
  • 出版时间:September 2014
  • 年:2014
  • 卷:41
  • 期:9
  • 页码:5877-5881
  • 全文大小:269 KB
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  • 作者单位:Sercan Ergun (1)
    Kaifee Arman (1)
    Ebru Temiz (1)
    ?brahim Bozgeyik (2)
    ?nder Yumruta? (2)
    Muhammad Safdar (1)
    Hasan Da?l? (1)
    Ahmet Arslan (1)
    Serdar Oztuzcu (1)

    1. Department of Medical Biology, Faculty of Medicine, Gaziantep University, ?ehitkamil, 27310, Gaziantep, Turkey
    2. Department of Medical Biology, Faculty of Medicine, Ad?yaman University, Ad?yaman, Turkey
  • ISSN:1573-4978
文摘
Caspases are important initiators and most well-known finishers of apoptosis. By changing the death propagation homeostatic equilibrium, their different expression patterns might trigger the progression of hazardous diseases like cancer. miR-221 is an oncogenic miRNA. It is known to have both anti-angiogenic and angiogenic effect. The aim of this work was to compare the expression levels of miR-221 and its target caspase-3 in different cancer cell lines and to find out a relationship between these two. We also tried to establish a prominent relationship between miR-221 and its role in apoptosis by studying their expression levels. Our results indicate that expression of caspase-3 is quite lower as compared to miR-221 expression in all of the selected cancer cell lines. As a result, we conclude that miR-221 may have a crucial role in repressing the expression of caspase-3 which may contribute to a lower apoptotic rate, thus supporting the selection of more aggressive cancer cells. To our knowledge, this is the first study related to the expression levels of caspase-3 and miR-221 in different cell lines at the same time. We expect that our study might pave the way for better understanding the role of miR-221 in apoptotic regulation of caspase-3.

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