1 Ocak 2014 Dergi makalesi Açık Erişim

Ai, Lingbao; Kim, Wan-Ju; Alpay, Merve; Tang, Ming; Pardo, Carolina E.; Hatakeyama, Shigetsugu; May, W. Stratford; Kladde, Michael P.; Heldermon, Coy D.; Siegel, Erin M.; Brown, Kevin D.

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{
  "@context": "https://schema.org/", 
  "@id": 63399, 
  "@type": "ScholarlyArticle", 
  "creator": [
    {
      "@type": "Person", 
      "name": "Ai, Lingbao"
    }, 
    {
      "@type": "Person", 
      "name": "Kim, Wan-Ju"
    }, 
    {
      "@type": "Person", 
      "name": "Alpay, Merve"
    }, 
    {
      "@type": "Person", 
      "name": "Tang, Ming"
    }, 
    {
      "@type": "Person", 
      "name": "Pardo, Carolina E."
    }, 
    {
      "@type": "Person", 
      "affiliation": "Hokkaido Univ, Grad Sch Med, Dept Biochem, Sapporo, Hokkaido, Japan", 
      "name": "Hatakeyama, Shigetsugu"
    }, 
    {
      "@type": "Person", 
      "name": "May, W. Stratford"
    }, 
    {
      "@type": "Person", 
      "name": "Kladde, Michael P."
    }, 
    {
      "@type": "Person", 
      "name": "Heldermon, Coy D."
    }, 
    {
      "@type": "Person", 
      "name": "Siegel, Erin M."
    }, 
    {
      "@type": "Person", 
      "name": "Brown, Kevin D."
    }
  ], 
  "datePublished": "2014-01-01", 
  "description": "TRIM29 (ATDC) exhibits a contextual function in cancer, but seems to exert a tumor-suppressor role in breast cancer. Here, we show that TRIM29 is often silenced in primary breast tumors and cultured tumor cells as a result of aberrant gene hypermethylation. RNAi-mediated silencing of TRIM29 in breast tumor cells increased their motility, invasiveness, and proliferation in a manner associated with increased expression of mesenchymal markers (N-cadherin and vimentin), decreased expression of epithelial markers (E-cadherin and EpCAM), and increased expression and activity of the oncogenic transcription factor TWIST1, an important driver of the epithelial-mesenchymal transition (EMT). Functional investigations revealed an inverse relationship in the expression of TRIM29 and TWIST1, suggesting the existence of a negative regulatory feedback loop. In support of this relationship, we found that TWIST1 inhibited TRIM29 promoter activity through direct binding to a region containing a cluster of consensus E-box elements, arguing that TWIST1 transcriptionally represses TRIM29 expression. Analysis of a public breast cancer gene-expression database indicated that reduced TRIM29 expression was associated with reduced relapse-free survival, increased tumor size, grade, and metastatic characteristics. Taken together, our results suggest that TRIM29 acts as a tumor suppressor in breast cancer through its ability to inhibit TWIST1 and suppress EMT. (C) 2014 AACR.", 
  "headline": "TRIM29 Suppresses TWIST1 and Invasive Breast Cancer Behavior", 
  "identifier": 63399, 
  "image": "https://aperta.ulakbim.gov.tr/static/img/logo/aperta_logo_with_icon.svg", 
  "license": "http://www.opendefinition.org/licenses/cc-by", 
  "name": "TRIM29 Suppresses TWIST1 and Invasive Breast Cancer Behavior", 
  "url": "https://aperta.ulakbim.gov.tr/record/63399"
}