Activation of the JNK/SAPK and P38 Mitogen-Activated Protein Kinase Signaling Pathways Sensitize Tumor Cells to Cisplatin-Induced Apoptosis | Zendy

Abdellah Mansouri | Zendy; Lon D. Ridgway | Zendy; Qingxiu Zhang | Zendy; François X. Claret | Zendy

Open Access

Activation of the JNK/SAPK and P38 Mitogen-Activated Protein Kinase Signaling Pathways Sensitize Tumor Cells to Cisplatin-Induced Apoptosis

Author(s) -

Abdellah Mansouri,

Lon D. Ridgway,

Qingxiu Zhang,

François X. Claret

Publication year - 2001

Publication title -

the scientific world journal

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.453

H-Index - 93

eISSN - 2356-6140

pISSN - 1537-744X

DOI - 10.1100/tsw.2001.159

Subject(s) - p38 mitogen activated protein kinases , apoptosis , cancer research , mitogen activated protein kinase , kinase , protein kinase a , cisplatin , ask1 , signal transduction , microbiology and biotechnology , protein kinase r , chemistry , mitogen activated protein kinase kinase , medicine , biology , chemotherapy , biochemistry

. Chemoresistance is a major impediment to the successful treatment of cancer. However, the mechanisms of chemoresistance are poorly understood. Cisplatin (CDDP) treatment activates multiple signal transduction pathways that can lead to diverse cellular responses, including cell cycle arrest (G2/M), DNA repair, or apoptosis. Differences in early signal transduction activity in response to chemotherapy could provide insight regarding the ultimate outcome of treatment. In this study, we attempted to elucidate the mechanisms of resistance to cisplatin in a cisplatin-sensitive human ovarian cancer cell line and a cisplatinresistant clone (2008 and 2008.C13 respectively).

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