1 Ocak 2023 Dergi makalesi Açık Erişim

Akkoc, Yunus; Dalci, Kubilay; Karakas, Hacer Ezgi; Erbil-Bilir, Secil; Yalav, Orcun; Sakman, Gurhan; Celik, Faruk; Arikan, Soykan; Zeybek, Umit; Ergin, Melek; Akkiz, Hikmet; Dilege, Ece; Dengjel, Joern; Dogan-Ekici, A. Isin; Gozuacik, Devrim

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/260143</identifier>
  <creators>
    <creator>
      <creatorName>Akkoc, Yunus</creatorName>
      <givenName>Yunus</givenName>
      <familyName>Akkoc</familyName>
    </creator>
    <creator>
      <creatorName>Dalci, Kubilay</creatorName>
      <givenName>Kubilay</givenName>
      <familyName>Dalci</familyName>
      <affiliation>Cukurova Univ, Fac Med, Dept Gen Surg, Adana, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Karakas, Hacer Ezgi</creatorName>
      <givenName>Hacer Ezgi</givenName>
      <familyName>Karakas</familyName>
      <affiliation>Sabanci Univ Nanotechnol Res &amp; Applicat Ctr SUNUM, Dept Biotechnol, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Erbil-Bilir, Secil</creatorName>
      <givenName>Secil</givenName>
      <familyName>Erbil-Bilir</familyName>
      <affiliation>Sabanci Univ Nanotechnol Res &amp; Applicat Ctr SUNUM, Dept Biotechnol, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Yalav, Orcun</creatorName>
      <givenName>Orcun</givenName>
      <familyName>Yalav</familyName>
      <affiliation>Cukurova Univ, Fac Med, Dept Gen Surg, Adana, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Sakman, Gurhan</creatorName>
      <givenName>Gurhan</givenName>
      <familyName>Sakman</familyName>
      <affiliation>Cukurova Univ, Fac Med, Dept Gen Surg, Adana, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Celik, Faruk</creatorName>
      <givenName>Faruk</givenName>
      <familyName>Celik</familyName>
      <affiliation>Istanbul Univ, Dept Mol Med, Aziz Sancar Inst Expt Med, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Arikan, Soykan</creatorName>
      <givenName>Soykan</givenName>
      <familyName>Arikan</familyName>
      <affiliation>Minist Hlth, Dept Gen Surg, Samatya Training &amp; Res Hosp, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Zeybek, Umit</creatorName>
      <givenName>Umit</givenName>
      <familyName>Zeybek</familyName>
      <affiliation>Istanbul Univ, Dept Mol Med, Aziz Sancar Inst Expt Med, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Ergin, Melek</creatorName>
      <givenName>Melek</givenName>
      <familyName>Ergin</familyName>
      <affiliation>Cukurova Univ, Fac Med, Dept Pathol, Adana, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Akkiz, Hikmet</creatorName>
      <givenName>Hikmet</givenName>
      <familyName>Akkiz</familyName>
      <affiliation>Cukurova Univ, Fac Med, Dept Gastroenterol, Adana, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Dilege, Ece</creatorName>
      <givenName>Ece</givenName>
      <familyName>Dilege</familyName>
    </creator>
    <creator>
      <creatorName>Dengjel, Joern</creatorName>
      <givenName>Joern</givenName>
      <familyName>Dengjel</familyName>
      <affiliation>Univ Fribourg, Dept Biol, Fribourg, Switzerland</affiliation>
    </creator>
    <creator>
      <creatorName>Dogan-Ekici, A. Isin</creatorName>
      <givenName>A. Isin</givenName>
      <familyName>Dogan-Ekici</familyName>
      <affiliation>Acibadem Mehmet Ali Aydinlar Univ, Dept Pathol, Sch Med, Istanbul, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Gozuacik, Devrim</creatorName>
      <givenName>Devrim</givenName>
      <familyName>Gozuacik</familyName>
    </creator>
  </creators>
  <titles>
    <title>Tumor-Derived Ctf1 (Cardiotrophin 1) Is A Critical Mediator Of Stroma-Assisted And Autophagy-Dependent Breast Cancer Cell Migration, Invasion And Metastasis</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2023</publicationYear>
  <dates>
    <date dateType="Issued">2023-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/260143</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1080/15548627.2022.2090693</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">Macroautophagy/autophagy is an evolutionarily conserved cellular stress response mechanism. Autophagy induction in the tumor microenvironment (stroma) has been shown to support tumor metabolism. However, cancer cell-derived secreted factors that initiate communication with surrounding cells and stimulate autophagy in the tumor microenvironment are not fully documented. We identified CTF1/CT-1 (cardiotrophin 1) as an activator of autophagy in fibroblasts and breast cancer-derived carcinoma-associated fibroblasts (CAFs). We showed that CTF1 stimulated phosphorylation and nuclear translocation of STAT3, initiating transcriptional activation of key autophagy proteins. Additionally, following CTF1 treatment, AMPK and ULK1 activation was observed. We provided evidence that autophagy was important for CTF1-dependent ACTA2/alpha-SMA accumulation, stress fiber formation and fibroblast activation. Moreover, promotion of breast cancer cell migration and invasion by activated fibroblasts depended on CTF1 and autophagy. Analysis of the expression levels of CTF1 in patient-derived breast cancer samples led us to establish a correlation between CTF1 expression and autophagy in the tumor stroma. In line with our in vitro data on cancer migration and invasion, higher levels of CTF1 expression in breast tumors was significantly associated with lymph node metastasis in patients. Therefore, CTF1 is an important mediator of tumor-stroma interactions, fibroblast activation and cancer metastasis, and autophagy plays a key role in all these cancer-related events.</description>
  </descriptions>
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