1 Ocak 2020 Dergi makalesi Açık Erişim

Agca, Can Ali; Kirici, Mahinur; Nedzvetsky, Victor S.; Gundogdu, Ramazan; Tykhomyrov, Artem A.

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{
  "@context": "https://schema.org/", 
  "@id": 10957, 
  "@type": "ScholarlyArticle", 
  "creator": [
    {
      "@type": "Person", 
      "affiliation": "Bingol Univ, Dept Mol Biol & Genet, TR-12000 Bingol, Turkey", 
      "name": "Agca, Can Ali"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Bingol Univ, Dept Chem, TR-12000 Bingol, Turkey", 
      "name": "Kirici, Mahinur"
    }, 
    {
      "@type": "Person", 
      "name": "Nedzvetsky, Victor S."
    }, 
    {
      "@type": "Person", 
      "affiliation": "Bingol Univ, Dept Biol, TR-12000 Bingol, Turkey", 
      "name": "Gundogdu, Ramazan"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Natl Acad Sci Ukraine, Dept Enzyme Chem & Biochem, Palladin Inst Biochem, UA-01030 Kiev, Ukraine", 
      "name": "Tykhomyrov, Artem A."
    }
  ], 
  "datePublished": "2020-01-01", 
  "description": "Resistance to chemotherapeutic drugs is a critical problem in cancer therapy, but the underlying mechanism has not been fully elucidated. TP53-induced glycolysis regulatory phosphatase (TIGAR), an important glycolysis and apoptosis regulator, plays a crucial role in cancer cell survival by protecting cells against oxidative stress-induced apoptosis. In the present study, we investigated whether TIGAR is involved in epithelial-mesenchymal transition (EMT) in doxorubicin (DOX)-resistant human non-small cell lung cancer (NSCLC), A549/DOX cells. We found that the expression of TIGAR was significantly higher in A549/DOX cells than in the parent A549 cell lines. siRNA-mediated TIGAR knockdown reduced migration, viability and colony survival of doxorubicin-resistant lung cancer cells. Also, TIGAR knockdown decreased pro-survival protein Bcl-2 and increased pro-apoptotic Bax and cleaved poly (ADP-ribose) polymerase (PARP). Moreover, TIGAR depletion significantly up-regulated both caspase-3 and caspase-9 expression. Furthermore, TIGAR depletion up-regulated the expression of E-cadherin and down-regulated the expression of vimentin. These results indicate that TIGAR knockdown may inhibit EMT in doxorubicin (DOX)-resistant human NSCLC and may represent a therapeutic target for a non-small lung cancer cells chemoresistance.", 
  "headline": "The Effect of TIGAR Knockdown on Apoptotic and Epithelial-Mesenchymal Markers Expression in Doxorubicin-Resistant Non-Small Cell Lung Cancer A549 Cell Lines", 
  "identifier": 10957, 
  "image": "https://aperta.ulakbim.gov.tr/static/img/logo/aperta_logo_with_icon.svg", 
  "license": "http://www.opendefinition.org/licenses/cc-by", 
  "name": "The Effect of TIGAR Knockdown on Apoptotic and Epithelial-Mesenchymal Markers Expression in Doxorubicin-Resistant Non-Small Cell Lung Cancer A549 Cell Lines", 
  "url": "https://aperta.ulakbim.gov.tr/record/10957"
}