دورية أكاديمية
Crosstalk from survival to necrotic death coexists in DU-145 cells by curcumin treatment.
| العنوان: | Crosstalk from survival to necrotic death coexists in DU-145 cells by curcumin treatment. |
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| المؤلفون: | Kang D; Institute for Cancer Research, College of Medicine, Yonsei University, Seoul, Republic of Korea., Park W, Lee S, Kim JH, Song JJ |
| المصدر: | Cellular signalling [Cell Signal] 2013 May; Vol. 25 (5), pp. 1288-300. Date of Electronic Publication: 2013 Jan 24. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Science Ltd Country of Publication: England NLM ID: 8904683 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-3913 (Electronic) Linking ISSN: 08986568 NLM ISO Abbreviation: Cell Signal Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Oxford : Elsevier Science Ltd Original Publication: Oxford ; New York : Pergamon Press, 1988- |
| مواضيع طبية MeSH: | Antineoplastic Agents/*toxicity , Apoptosis/*drug effects , Curcumin/*toxicity, Caspases/metabolism ; Cell Line ; Cell Survival/drug effects ; Humans ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases/metabolism ; Necrosis/metabolism ; Phosphorylation ; Reactive Oxygen Species/metabolism ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases/metabolism |
| مستخلص: | Curcumin as an anticancer agent was investigated in regards to its ability to regulate the switching of cancer cells from survival to necrotic cell death. At higher concentrations, curcumin induced ROS production leading to JNK and p38 phosphorylation in DU-145 prostate cancer cells. Of the MAP kinases, ERK or p38/JNK were phosphorylated earlier during curcumin treatment, and were responsible for curcumin-induced cell survival at early time of treatment with the help of phosphorylated Akt, while significant amounts of ROS production in later periods stimulated cell death with caspase degradation. In addition to autophagic signaling, necrosis was dominant with little apoptotic cell death. Caspase activation was completely prohibited by procaspase degradation, which contributed to curcumin-induced early necrosis. At the later incubation period (24h), cytotoxicity caused by curcumin peaked, at which time survival or proliferation signals, such as phosphorylated Akt and phosphorylated ERK, was almost completely diminished. Curcumin-induced ROS were shown to function, biphasically depending on the incubation period; facilitating survival, in the earlier incubation period, and necrotic death in the later. Based on all of these results, we concluded that curcumin contributes to a complex signaling network, affecting cell survival and necrotic cell death, which in turn could inhibit apoptotic cell death. (Copyright © 2013 Elsevier Inc. All rights reserved.) |
| المشرفين على المادة: | 0 (Antineoplastic Agents) 0 (Reactive Oxygen Species) EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases) EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) EC 3.4.22.- (Caspases) IT942ZTH98 (Curcumin) |
| تواريخ الأحداث: | Date Created: 20130129 Date Completed: 20131018 Latest Revision: 20131121 |
| رمز التحديث: | 20231215 |
| DOI: | 10.1016/j.cellsig.2013.01.014 |
| PMID: | 23353183 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1873-3913 |
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| DOI: | 10.1016/j.cellsig.2013.01.014 |