MicroRNA-206 suppresses gastric cancer cell growth and metastasis
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  • 作者:Jun Ren (1) (2)
    Hui-jie Huang (2)
    Yu Gong (1)
    Shen Yue (2)
    Li-ming Tang (1)
    Steven Y Cheng (2)

    1. Department of General Surgery
    ; Nanjing Medical University affiliated Changzhou No. 2 Hospital ; 213000 ; Changzhou ; Jiangsu ; PR. China
    2. Department of Developmental Genetics
    ; School of Basic Medical Sciences ; Nanjing Medical University ; 210029 ; Nanjing ; Jiangsu ; PR. China
  • 关键词:Gastric cancer ; miR ; 206 ; Metastasis ; Tumor suppressor
  • 刊名:Cell & Bioscience
  • 出版年:2014
  • 出版时间:December 2014
  • 年:2014
  • 卷:4
  • 期:1
  • 全文大小:1,418 KB
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  • 刊物主题:Cell Biology; Microbiology;
  • 出版者:BioMed Central
  • ISSN:2045-3701
文摘
Gastric cancer is one of the leading causes of cancer death world-wide and carries a high rate of metastatic risk. In addition to other protein-coding oncogenes and tumor suppressor genes, microRNAs play an important role in gastric cancer tumorigenic progression. Here, we show that miR-206 is expressed at markedly low levels in a cohort of gastric tumors compared to their matching normal tissues, and in a number of gastric cancer cell lines. Down-regulation of miR-206 was particularly significant in tumors with lymphatic metastasis, local invasion, and advanced TNM staging. We find that forced expression of miR-206 suppressed the proliferation, colony-formation, and xenograft tumorigenesis of SCG-7901 cells, a line of gastric cancer cells. Forced expression of miR-206 also suppressed SCG-7901 cell migration and invasion, as well as metastasis in cell culture or tail-vein injected mouse models, respectively. The anti-metastatic effect of miR-206 is likely mediated by targeting metastasis regulatory genes STC2, HDAC4, KLF4, IGF1R, FRS2, SFRP1, BCL2, BDNF, and K-ras, which were drastically down-regulated by stable expression of exogenous miR-206 in SCG-7901 cells. Taken together, our results indicate that miR-206 is a tumor suppressor of gastric cancer acting at steps that regulate metastasis.

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