Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib
المؤلفون المشاركون
Blasiak, Janusz
Synowiec, Ewelina
Hoser, Grazyna
Bialkowska-Warzecha, Jolanta
Skorski, Tomasz
Pawlowska, Elzbieta
المصدر
العدد
المجلد 2015، العدد 2015 (31 ديسمبر/كانون الأول 2015)، ص ص. 1-9، 9ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2015-11-04
دولة النشر
مصر
عدد الصفحات
9
التخصصات الرئيسية
الملخص EN
Imatinib resistance is an emerging problem in the therapy of chronic myeloid leukemia (CML).
Because imatinib induces apoptosis, which may be coupled with mitochondria and DNA damage is a prototype apoptosis-inducing factor, we hypothesized that imatinib-sensitive and -resistant CML cells might differentially express apoptosis-related mitochondrially encoded genes in response to genotoxic stress.
We investigated the effect of doxorubicin (DOX), a DNA-damaging anticancer drug, on apoptosis and the expression of the mitochondrial NADH dehydrogenase 3 (MT-ND3) and cytochrome b (MT-CYB) in model CML cells showing imatinib resistance caused by Y253H mutation in the BCR-ABL1 gene (253) or culturing imatinib-sensitive (S) cells in increasing concentrations of imatinib (AR).
The imatinib-resistant 253 cells displayed higher sensitivity to apoptosis induced by 1 μM DOX and this was confirmed by an increased activity of executioner caspases 3 and 7 in those cells.
Native mitochondrial potential was lower in imatinib-resistant cells than in their sensitive counterparts and DOX lowered it.
MT-CYB mRNA expression in 253 cells was lower than that in S cells and 0.1 μM DOX kept this relationship.
In conclusion, imatinib resistance may be associated with altered mitochondrial response to genotoxic stress, which may be further exploited in CML therapy in patients with imatinib resistance.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Synowiec, Ewelina& Hoser, Grazyna& Bialkowska-Warzecha, Jolanta& Pawlowska, Elzbieta& Skorski, Tomasz& Blasiak, Janusz. 2015. Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib. BioMed Research International،Vol. 2015, no. 2015, pp.1-9.
https://search.emarefa.net/detail/BIM-1056341
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Synowiec, Ewelina…[et al.]. Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib. BioMed Research International No. 2015 (2015), pp.1-9.
https://search.emarefa.net/detail/BIM-1056341
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Synowiec, Ewelina& Hoser, Grazyna& Bialkowska-Warzecha, Jolanta& Pawlowska, Elzbieta& Skorski, Tomasz& Blasiak, Janusz. Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib. BioMed Research International. 2015. Vol. 2015, no. 2015, pp.1-9.
https://search.emarefa.net/detail/BIM-1056341
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1056341
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر