Chemosensitization of tumor cells: inactivation of nuclear factor-kappa B associated with chemosensitivity in melanoma cells after combination treatment with E2F-1 and doxorubicin.
Chemosensitization of tumor cells: inactivation of nuclear factor-kappa B associated with chemosensitivity in melanoma cells after combination treatment with E2F-1 and doxorubicin.
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DOI：
10.1007/978-1-59745-561-9_16
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发表时间：
2009
影响因子：
--
通讯作者：
H. Hao;H. Zhou;K. McMasters
中科院分区：
文献类型：
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作者：
H. Hao;H. Zhou;K. McMasters
联合化疗已被证明比单药治疗对许多类型的癌症更有效，但已知两者都会诱导癌细胞的耐药性。核因子-κB（NF-κB）和多药耐药（MDR）基因是导致耐药的两个主要因素。出于这个原因，化学基因治疗正在成为传统化疗组合的可行替代方案。我们已经表明，在黑色素瘤细胞中转导E2 F-1基因显著增加细胞对阿霉素的敏感性，从而对黑色素瘤细胞凋亡产生协同作用。基因芯片结果显示，E2 F-1和阿霉素联合作用后，NF-κB通路及相关基因发生了显著变化。事实上，NF-κB的失活与E2 F-1和阿霉素诱导的黑素瘤细胞凋亡相关，从而提供了NF-κB信号通路与该处理后黑素瘤细胞的化学敏感性之间的联系。
Combination chemotherapy has been shown to be more effective than single-agent therapy for many types of cancer, but both are known to induce drug resistance in cancer cells. Two major culprits in the development of this drug resistance are nuclear factor-κB (NF-κB) and the multidrug resistance (MDR) gene. For this reason, chemogene therapy is emerging as a viable alternative to conventional chemotherapy combinations. We have shown that transduction of the E2F-1 gene in melanoma cells markedly increases cell sensitivity to doxorubicin, thereby producing a synergistic effect on melanoma cell apoptosis. Our microarray results show that the NF-κB pathway and related genes undergo significant changes after the combined treatment of E2F-1 and doxorubicin. In fact, inactivation of NF-κB is associated with melanoma cell apoptosis induced by E2F-1 and doxorubicin, providing a link between the NF-κB signaling pathway and the chemosensitivity of melanoma cells after this treatment.