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首页> 外文期刊>Breast cancer research and treatment. >JNK/SAPK mediates doxorubicin-induced differentiation and apoptosis in MCF-7 breast cancer cells.
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JNK/SAPK mediates doxorubicin-induced differentiation and apoptosis in MCF-7 breast cancer cells.

机译：JNK / SAPK介导阿霉素诱导的MCF-7乳腺癌细胞分化和凋亡。

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摘要

Pharmacologic induction of cancer cell differentiation has potential in the treatment of breast cancer. Doxorubicin, a widely used anthracycline antibiotic, was previously reported to induce differentiation of MCF-7 breast cancer cells. We demonstrate in this study that inhibition of MCF-7 breast cancer cell growth by low dose doxorubicin (0.01 microg/ml) was accompanied by an increase in cytokeratin 8/18 and milk fat globule membrane protein expression, biomarkers for differentiation of breast cancer, as well as an increase in JNK/SAPK phosphorylation. High dose doxorubicin (10.0 microg/ml) induced apoptosis in these cells. Overexpression of dominant-inhibitory forms of JNK1 and c-Jun blocked both the differentiation and apoptotic effects of doxorubicin. These results suggest that JNK/SAPK pathway signaling plays a prominent role in doxorubicin-induced cell cycle withdrawal, differentiation and control of apoptosis in this cell system. These findings support the possibility that JNK/SAPK pathway activation may be a means of therapeutic intervention in breast cancer.
机译：癌细胞分化的药理诱导作用在乳腺癌的治疗中具有潜力。以前有报道称阿霉素是一种广泛使用的蒽环类抗生素，可诱导MCF-7乳腺癌细胞分化。我们在这项研究中证明，低剂量阿霉素（0.01 microg / ml）对MCF-7乳腺癌细胞生长的抑制作用伴随着细胞角蛋白8/18和乳脂球膜蛋白表达的增加，乳腺癌分化的生物标志物，以及JNK / SAPK磷酸化的增加。大剂量阿霉素（10.0微克/毫升）诱导这些细胞凋亡。 JNK1和c-Jun的显性抑制形式的过表达可阻断阿霉素的分化和凋亡作用。这些结果表明，JNK / SAPK途径信号传导在阿霉素诱导的细胞周期退出，该细胞系统的分化和细胞凋亡控制中起着重要作用。这些发现支持了JNK / SAPK途径激活可能是乳腺癌治疗干预手段的可能性。

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