https://scholars.lib.ntu.edu.tw/handle/123456789/494639
標題: | Basal levels and patterns of anticancer drug-induced activation of nuclear factor-kappaB (NF-kappaB), and its attenuation by tamoxifen, dexamethasone, and curcumin in carcinoma cells | 作者: | Chuang S.-E. Yeh P.-Y. YEN-SHEN LU Lai G.-M. Liao C.-M. Gao M. ANN-LII CHENG |
公開日期: | 2002 | 卷: | 63 | 期: | 9 | 起(迄)頁: | 1709-1716 | 來源出版物: | Biochemical Pharmacology | 摘要: | Nuclear factor-κB (NF-κB) has been implicated in the development of drug resistance in cancer cells. We systematically examined the baseline levels of NF-κB activity of representative carcinoma cell lines, and the change of NF-κB activity in response to a challenge with four major anticancer drugs (doxorubicin, 5-fluorouracil, cisplatin, and paclitaxel). We found that the basal level of NF-κB activity was heterogeneous and roughly correlated with drug resistance. When challenged with various drugs, all the cell lines examined responded with a transient activation of NF-κB which then declined to basal level despite variation in the concentration of the agent and the timing of the treatment. In contrast to tumor necrosis factor-α (TNF-α), which activates NF-κB in minutes, NF-κB activation induced by anticancer drugs usually occurred more than 1hr after stimulation. A gradual increase of total NF-κB and its nuclear translocation, and cytoplasmic translocation of nuclear IκBα and its degradation were involved in this process. In particular, when cells were pretreated with common biologic modulators such as tamoxifen, dexamethasone, and curcumin, the doxorubicin-induced NF-κB activation was attenuated significantly. This inhibition may play a role in sensitizing cancer cells to chemotherapeutic drugs. This study has demonstrated that activation of NF-κB is a general cellular response to anticancer drugs, and the mechanism of activation appears to be distinct from that induced by TNF-α. These observations may have implications for improving the efficacy of systemic chemotherapy for cancer patients. ? 2002 Elsevier Science Inc. All rights reserved. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036569563&doi=10.1016%2fS0006-2952%2802%2900931-0&partnerID=40&md5=66c265ba7c59c3a6da54f3f471a3df40 https://scholars.lib.ntu.edu.tw/handle/123456789/494639 |
ISSN: | 0006-2952 | DOI: | 10.1016/S0006-2952(02)00931-0 | SDG/關鍵字: | cisplatin; curcumin; dexamethasone; doxorubicin; fluorouracil; immunoglobulin enhancer binding protein; paclitaxel; tamoxifen; tumor necrosis factor alpha; antineoplastic activity; article; cancer cell; cancer research; carcinoma cell; cell assay; cell line; cell nucleus; cell stimulation; concentration (parameters); controlled study; correlation analysis; cytoplasm; drug efficacy; drug response; human; human cell; intracellular transport; priority journal; protein analysis; protein degradation; protein determination; protein transport; provocation test; sensitization; time; Active Transport, Cell Nucleus; Antineoplastic Agents; Curcumin; Dexamethasone; DNA-Binding Proteins; Doxorubicin; Drug Hypersensitivity; Drug Interactions; Humans; I-kappa B Proteins; NF-kappa B; Tamoxifen; Tetradecanoylphorbol Acetate; Tumor Cells, Cultured |
顯示於: | 醫學院附設醫院 (臺大醫院) |
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