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Sensitization of U937 leukemia cells to doxorubicin by the MG132 proteasome inhibitor induces an increase in apoptosis by suppressing NF-kappa B and mitochondrial membrane potential loss

机译:MG132蛋白酶体抑制剂对U937白血病细胞对阿霉素的敏感性可通过抑制NF-κB和线粒体膜电位损失而诱导凋亡增加

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摘要

BackgroundThe resistance of cancerous cells to chemotherapy remains the main limitation for cancer treatment at present. Doxorubicin (DOX) is a potent antitumor drug that activates the ubiquitin-proteasome system, but unfortunately it also activates the Nuclear factor kappa B (NF-кB) pathway leading to the promotion of tumor cell survival. MG132 is a drug that inhibits I kappa B degradation by the proteasome-avoiding activation of NF-кB. In this work, we studied the sensitizing effect of the MG132 proteasome inhibitor on the antitumor activity of DOX.
机译:背景技术癌细胞对化学疗法的抗性仍然是目前癌症治疗的主要限制。阿霉素(DOX)是一种有效的抗肿瘤药物,可激活泛素-蛋白酶体系统,但不幸的是,它也可激活核因子κB(NF-кB)途径,从而促进肿瘤细胞存活。 MG132是通过避免蛋白酶体激活NF-кB抑制IκB降解的药物。在这项工作中,我们研究了MG132蛋白酶体抑制剂对DOX的抗肿瘤活性的增敏作用。

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