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Enhancing responsiveness of pancreatic cancer cells to gemcitabine treatment under hypoxia by heme oxygenase-1 inhibition

Abdalla, Maher Y ; Ahmad, Iman M ; Rachagani, Satyanarayana ; Banerjee, Kasturi ; Thompson, Christopher M ; Maurer, Hans C ; Olive, Kenneth P ; Bailey, Katie L ; Britigan, Bradley E ; Kumar, Sushil

Translational research : the journal of laboratory and clinical medicine, 04 January 2019 [Rivista Peer Reviewed]

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  • Titolo:
    Enhancing responsiveness of pancreatic cancer cells to gemcitabine treatment under hypoxia by heme oxygenase-1 inhibition
  • Autore: Abdalla, Maher Y ; Ahmad, Iman M ; Rachagani, Satyanarayana ; Banerjee, Kasturi ; Thompson, Christopher M ; Maurer, Hans C ; Olive, Kenneth P ; Bailey, Katie L ; Britigan, Bradley E ; Kumar, Sushil
  • Note di contenuto: Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies and has one of the worst prognoses leading to a meager 5-year survival rate of ∼8%. Chemotherapy has had limited success in extending the life span of patients with advanced PDAC due to poor tumor perfusion and hypoxia-induced resistance. Hypoxia reprograms the gene expression profile and upregulates the expression of multiple genes including heme oxygenase-1 (HO-1), which provide survival advantage to PDAC cells. However, the relationships between HO-1, hypoxia, and response to chemotherapy is unclear. Our results showed that hypoxia upregulates the expression of HO-1 in PDAC cells, and HO-1 inhibition using the HO-1 inhibitors zinc protoporphyrin, tin protoporphyrin IX (SnPP), and HO-1 knockout using CRISPR/Cas9 suppresses the proliferation of PDAC cells under hypoxia and sensitize them to gemcitabine under in vitro conditions. Treating orthotopic tumors with SnPP, or SnPP in combination with gemcitabine,...
  • Fa parte di: Translational research : the journal of laboratory and clinical medicine, 04 January 2019
  • Soggetti: Gemcitabine ; Heme Oxygenase-1 (Ho-1) ; Pancreatic Ductal Adenocarcinoma (Pdac) ; Snpp ; Znpp
  • Lingua: Inglese
  • Tipo: Articolo
  • Identificativo: E-ISSN: 1878-1810 ; PMID: 30653942 Version:1 ; DOI: 10.1016/j.trsl.2018.12.008

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