双硫仑/铜复合物抑制 NFkappaB 活性并增强吉西他滨对结肠和乳腺癌细胞系的细胞毒性作用。
Disulfiram/copper complex inhibiting NFkappaB activity and potentiating cytotoxic effect of gemcitabine on colon and breast cancer cell lines.
机构信息
Research Institute in Healthcare Science, University of Wolverhampton, UK.
出版信息
Cancer Lett. 2010 Apr 1;290(1):104-13. doi: 10.1016/j.canlet.2009.09.002. Epub 2009 Sep 25.
Most of the gemcitabine (dFdC) resistant cell lines manifested high NFkappaB activity. The NFkappaB activity can be induced by dFdC and 5-FU exposure. The chemosensitizing effect of disulfiram (DS), an anti-alcoholism drug and NFkappaB inhibitor, and copper (Cu) on the chemoresistant cell lines was examined. The DS/Cu complex significantly enhanced the cytotoxicity of dFdC (resistant cells: 12.2-1085-fold) and completely reversed the dFdC resistance in the resitant cell lines. The dFdC-induced NFkappaB activity was markedly inhibited by DS/Cu complex. The data from this study indicated that DS may be used in clinic to improve the therapeutic effect of dFdC in breast and colon cancer patients.
大多数吉西他滨（dFdC）耐药细胞系表现出高 NFkappaB 活性。NFkappaB 活性可被 dFdC 和 5-FU 暴露诱导。本研究检测了戒酒药物和 NFkappaB 抑制剂双硫仑（DS）以及铜（Cu）对耐药细胞系的化疗增敏作用。DS/Cu 复合物显著增强了 dFdC 的细胞毒性（耐药细胞：12.2-1085 倍），并完全逆转了耐药细胞系中的 dFdC 耐药性。DS/Cu 复合物显著抑制了 dFdC 诱导的 NFkappaB 活性。本研究数据表明，DS 可用于临床，以提高乳腺癌和结肠癌患者接受 dFdC 治疗的效果。
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