کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5861365 | 1133760 | 2015 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Acute myeloid leukemia cells MOLM-13 and SKM-1 established for resistance by azacytidine are crossresistant to P-glycoprotein substrates
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کلمات کلیدی
CDNBAMLCisptAzacytidineP-gpAzaCVCRMitoxantroneMTXMDSGSTDOXMDRNF-κB1-chloro-2,4-dinitrobenzene - 1-کلرو-2،4-دینیتروبنزنP-glycoprotein - P-گلیکوپروتئینDoxorubicin - دوکسوروبیسینmyelodysplastic syndrome - سندرم میلودیسپلاستیکcisplatin - سیس پلاتینacute myeloid leukemia - لوسمی حاد میلوئیدی یا به اختصار AMLVer - مشاهده کنیدDrug resistance - مقاومت داروییMultidrug resistance - مقاومت چند داروییVerapamil - وراپامیلvincristine - وین کریستینglutathione S-transferase - گلوتاتیون S-ترانسفراز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Establishment of the acute myeloid leukemia cells SKM-1 and MOLM-13 for resistance by azacytidine (AzaC) resulted in SKM-1/AzaC and MOLM-13/AzaC cell variants with reduced sensitivity to AzaC. Despite the fact that AzaC is not substrate of P-glycoprotein (P-gp), the adaptation procedure resulted in an induction in P-gp expression/efflux activity that confers crossresistance to P-gp substrates in both resistant cell variants. While the resistance to P-gp substrates in SKM-1/AzaC and MOLM-13/AzaC cells could be reversed by the P-gp inhibitors, resistance to AzaC was insensitive to these inhibitors in both resistant cell variants. In addition, NF-κB and the antiapoptotic protein Bcl-2 were downregulated and the proapoptotic proteins Bax and p53 were upregulated in both resistant cell variants when compared with their sensitive counterparts. Moreover, at least five times the elevation in overall glutathione S-transferase activity was measured with 1-chloro-2, 5-dinitrobenzene as a substrate in the resistant variant of both cell lines. Taken together, the findings of the present study indicate that the treatment of AML cells with AzaC might lead to a drug resistance phenotype that may be associated with cross resistance to P-gp substrates and substrates of glutathione S-transferases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology in Vitro - Volume 29, Issue 7, October 2015, Pages 1405-1415
Journal: Toxicology in Vitro - Volume 29, Issue 7, October 2015, Pages 1405-1415
نویسندگان
Lucia Messingerova, Denisa Imrichova, Helena Kavcova, Katarina Turakova, Albert Breier, Zdena Sulova,