Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. MDR glioblastoma cell lines were created in response to prolonged doxorubicin chemotherapy. [[CD133]], [[DNA dependent protein kinase]] (DNA-PK) and [[MDR protein 1]] (MDR1) were markedly elevated in these cells. CD133 and DNA-PK may increase MDR1 via the [[phosphoinositide 3 kinase]] (PI3K)-[[Akt]] [[signaling pathway]]. PI3K downstream targets Akt and [[nuclear factor]] [[NF-κB]], which interacts with the MDR1 promoter, were also elevated in these cells. Downregulation of CD133 and DNA-PK by small interfering RNA, or inhibition of PI3K or Akt, decreased Akt, NF-κB and MDR1 expression. The results indicate that CD133 and DNA-PK regulate MDR1 through the PI3K- or Akt-NF-κB signal pathway. Consequently, a novel chemotherapeutic regimen targeting CD133 and DNA-PK in combination with traditional protocols may increase chemotherapeutic efficacy and improve prognosis for individuals who present with glioblastoma ((Xi G, Hayes E, Lewis R, Ichi S, Mania-Farnell B, Shim K, Takao T, Allender E, Mayanil CS, Tomita T. CD133 and DNA-PK regulate MDR1 via the PI3K- or Akt-NF-κB pathway in multidrug-resistant glioblastoma cells in vitro. Oncogene. 2015 Mar 30. doi: 10.1038/onc.2015.78. [Epub ahead of print] PubMed PMID: 25823028.)). mdr_glioblastoma_cell_line.txt Last modified: 2024/06/07 02:59by 127.0.0.1