Academic Journal

التفاصيل البيبلوغرافية
العنوان: [Untitled]
المؤلفون: Ying-Ying Xu, Ting-Ting Wu, Shui-Hong Zhou, Yang-Yang Bao, Qin-Ying Wang, Jun Fan, Ya-Ping Huang, Dr Shui-Hong Zhou
المساهمون: The Pennsylvania State University CiteSeerX Archives
المصدر: http://www.ijcep.com/files/ijcep0000889.pdf.
سنة النشر: 2014
المجموعة: CiteSeerX
الوصف: Glucose transporter-1 (GLUT-1) and PI3K/Akt are known to be closely involved in resistance to chemotherapy. Co-targeted therapy reducing GLUT-1 expression and PI3K/Akt pathway activity may overcome the chemoresistance of human cancers. Apigenin may inhibit the expression of GLUT-1 and the PI3K/Akt pathway. We hypothesized that over-expression of GLUT-1 and p-Akt was associated with the resistance to cisplatin of laryngeal carcinoma Hep-2 cells. We explored whether apigenin inhibited GLUT-1 and p-Akt, resulting in sensitization of laryngeal carcinoma Hep-2 cells to cisplatin. Real-time RT-PCR and Western blotting confirmed the presence of GLUT-1 mRNA, and GLUT-1 and p-Akt proteins in Hep-2 cells. We found that resistance or insensitivity of Hep-2 cells to cisplatin might be associated with such expression. Apigenin markedly enhanced the cisplatin-induced suppression of Hep-2 cell growth. This effect was concentration-and time-dependent. Thus apigenin may significantly reduce the levels of GLUT-1 mRNA, and GLUT-1 and p-Akt proteins, in cisplatin-treated Hep-2 cells, in a concentration-and timedependent manner. To conclude, overexpression of GLUT-1 mRNA may be associated with the resistance to cisplatin of laryngeal carcinoma Hep-2 cells. Apigenin may enhance the sensitivity to cisplatin of laryngeal carcinoma cells via inhibition of GLUT-1 and p-Akt expression.
نوع الوثيقة: text
وصف الملف: application/pdf
اللغة: English
Relation: http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.1060.534; http://www.ijcep.com/files/ijcep0000889.pdf
الاتاحة: http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.1060.534
http://www.ijcep.com/files/ijcep0000889.pdf
Rights: Metadata may be used without restrictions as long as the oai identifier remains attached to it.
رقم الانضمام: edsbas.F02A571B
قاعدة البيانات: BASE