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Mir-155 promotes cervical cancer cell proliferation through suppression of its target gene LKB1
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  • 作者:Guoying Lao (1)
    Ping Liu (1)
    Qiongwei Wu (1)
    Wenying Zhang (1)
    Yu Liu (1)
    Longtao Yang (1)
    Chengbin Ma (1)
  • 关键词:Cervical cancer ; Cell proliferation ; miR ; 155 ; LKB1
  • 刊名:Tumor Biology
  • 出版年:2014
  • 出版时间:December 2014
  • 年:2014
  • 卷:35
  • 期:12
  • 页码:11933-11938
  • 全文大小:547 KB
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  • 作者单位:Guoying Lao (1)
    Ping Liu (1)
    Qiongwei Wu (1)
    Wenying Zhang (1)
    Yu Liu (1)
    Longtao Yang (1)
    Chengbin Ma (1)

    1. Department of Gynecology, Changning Maternity and Infant Health Hospital of Shanghai, 773 Wuyi Road, Shanghai, 200051, China
  • 刊物主题:Cancer Research;
  • 出版者:Springer Netherlands
  • ISSN:1423-0380
文摘
MicroRNAs (miRNAs) are important regulators of many physiological and pathological processes, including cell proliferation, apoptosis, and cell cycle arrest. In this study, we aimed to investigate the biological role of miR-155 in cervical cancer and the underlying molecular mechanism involved in tumorigenesis. The expression of miR-155 in human cervical cancer tissues was detected by real-time PCR. MTT assay and BrdU incorporation assay were used to measure the proliferation of cervical cancer cells. Apoptosis cells and cell cycle distribution were analyzed by flow cytometry. We found that the expression of miR-155 was upregulated in cervical cancer tissues compared to the adjacent non-cancer tissues. Overexpression of miR-155 promoted the proliferation of Hela and SiHa cells. By contrast, downregulation of miR-155 inhibited the growth of cervical cancer cells. Flow cytometry analysis showed that low expression of miR-155 promoted apoptosis and induced cell cycle arrest in Hela and SiHa cells. Moreover, the mRNA and protein expression of LKB1 was significantly reduced in cervical cancer tissues. Luciferase reporter assay demonstrated that LKB1 was a target gene of miR-155, suggesting that miRNA-155 promoted the proliferation of cervical cancer cells by regulating LKB1 expression.

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