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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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/63399</identifier>
  <creators>
    <creator>
      <creatorName>Ai, Lingbao</creatorName>
      <givenName>Lingbao</givenName>
      <familyName>Ai</familyName>
    </creator>
    <creator>
      <creatorName>Kim, Wan-Ju</creatorName>
      <givenName>Wan-Ju</givenName>
      <familyName>Kim</familyName>
    </creator>
    <creator>
      <creatorName>Alpay, Merve</creatorName>
      <givenName>Merve</givenName>
      <familyName>Alpay</familyName>
    </creator>
    <creator>
      <creatorName>Tang, Ming</creatorName>
      <givenName>Ming</givenName>
      <familyName>Tang</familyName>
    </creator>
    <creator>
      <creatorName>Pardo, Carolina E.</creatorName>
      <givenName>Carolina E.</givenName>
      <familyName>Pardo</familyName>
    </creator>
    <creator>
      <creatorName>Hatakeyama, Shigetsugu</creatorName>
      <givenName>Shigetsugu</givenName>
      <familyName>Hatakeyama</familyName>
      <affiliation>Hokkaido Univ, Grad Sch Med, Dept Biochem, Sapporo, Hokkaido, Japan</affiliation>
    </creator>
    <creator>
      <creatorName>May, W. Stratford</creatorName>
      <givenName>W. Stratford</givenName>
      <familyName>May</familyName>
    </creator>
    <creator>
      <creatorName>Kladde, Michael P.</creatorName>
      <givenName>Michael P.</givenName>
      <familyName>Kladde</familyName>
    </creator>
    <creator>
      <creatorName>Heldermon, Coy D.</creatorName>
      <givenName>Coy D.</givenName>
      <familyName>Heldermon</familyName>
    </creator>
    <creator>
      <creatorName>Siegel, Erin M.</creatorName>
      <givenName>Erin M.</givenName>
      <familyName>Siegel</familyName>
    </creator>
    <creator>
      <creatorName>Brown, Kevin D.</creatorName>
      <givenName>Kevin D.</givenName>
      <familyName>Brown</familyName>
    </creator>
  </creators>
  <titles>
    <title>Trim29 Suppresses Twist1 And Invasive Breast Cancer Behavior</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2014</publicationYear>
  <dates>
    <date dateType="Issued">2014-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/63399</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1158/0008-5472.CAN-13-3579</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">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.</description>
  </descriptions>
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