首页> 美国卫生研究院文献>Journal of Oncology >TJ-41 Induces Apoptosis and Potentiates the Apoptotic Effects of 5-FU in Breast Cancer Cell Lines
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TJ-41 Induces Apoptosis and Potentiates the Apoptotic Effects of 5-FU in Breast Cancer Cell Lines

机译:TJ-41诱导5-FU在乳腺癌细胞株中的凋亡并增强其凋亡作用。

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摘要

Recent studies suggest that TJ-41, a herbal drug, possesses chemotherapeutic effects. Accordingly, this study was undertaken to investigate the anticarcinogenic effects of TJ-41 on human breast cancer cells lines. TJ-41 inhibited the proliferation of human breast cancer cell lines dose dependently. Flow cytometric analysis showed that this decrease in DNA synthesis is to be associated with induction of apoptosis. In both cell lines, apoptosis was abolished by caspase-9 inhibitor Z-LEHD-fmk but was weakly inhibited by caspase-8 inhibitor Z-IETD-fmk, indicating that caspase-9 activation was involved in TJ-41 induced apoptosis. Additionally, TJ-41 stimulated phosphorylation of c-Jun NH2-terminal kinase (JNK) and pretreatment of breast cancer cells with JNK inhibitor SP600125 completely abolished TJ-41 induced apoptosis. Our data also demonstrate that combined treatment of TJ-41 and 5-FU significantly potentiates the apoptotic effects of 5-FU in both breast cancer cell lines. Taken together, these data suggest that TJ-41 might provide a novel chemotherapeutic treatment for breast cancer.
机译:最近的研究表明,草药TJ-41具有化学治疗作用。因此,进行这项研究以研究TJ-41对人乳腺癌细胞系的抗癌作用。 TJ-41剂量依赖性地抑制人乳腺癌细胞系的增殖。流式细胞仪分析表明,DNA合成的这种减少与细胞凋亡的诱导有关。在这两种细胞系中,凋亡均被caspase-9抑制剂Z-LEHD-fmk消除,但被caspase-8抑制剂Z-IETD-fmk弱抑制,表明caspase-9激活与TJ-41诱导的凋亡有关。另外,TJ-41刺激c-Jun NH2末端激酶(JNK)的磷酸化,并用JNK抑制剂SP600125预处理乳腺癌细胞完全废除了TJ-41诱导的细胞凋亡。我们的数据还证明,联合治疗TJ-41和5-FU可以显着增强两种乳腺癌细胞系中5-FU的凋亡作用。综上所述,这些数据表明TJ-41可能为乳腺癌提供一种新颖的化学治疗方法。

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