Estradiol induces JNK-dependent apoptosis in glioblastoma cells

被引:29
作者
Altiok, Nedret [1 ]
Ersoz, Melike [2 ]
Koyuturk, Meral [3 ]
机构
[1] Yeni Yuzyil Univ, Sch Med, Dept Pharmacol, Yilanli Ayazma Caddesi 26, Istanbul, Turkey
[2] Istanbul Sci Bilim Univ, Inst Med Sci, Istanbul, Turkey
[3] Istanbul Sci Bilim Univ, Dept Histol & Embryol, Istanbul, Turkey
关键词
apoptosis; JNK/c-Jun; cancer therapy; estradiol; glioblastoma; N-TERMINAL KINASE; C6; GLIOMA-CELLS; ESTROGEN; PATHWAY; BRAIN; DEATH; ACTIVATION; INHIBITOR; MECHANISM; AGENTS;
D O I
10.3892/ol.2011.385
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Estrogens exert multiple regulatory actions on cellular events in a variety of tissues including the brain. In the present study, the signaling mechanisms of the concentration-dependent effects of 17-beta-estradiol (estradiol) on glioblastoma cells were investigated. Cell viability was evaluated by the trypan blue exclusion assay. Cell growth and kinase activities were evaluated by immunocytochemistry and Western blotting. The results showed that high concentrations of estradiol inhibit growth and induce apoptosis in C6 rat glioma and T98G human glioblastoma cells. The blockade of the c-jun NH2-terminal kinase (JNK) signaling pathway prevented these effects of estradiol, indicating the critical role of the JNK/c-jun signaling cascade in glioblastoma cell growth inhibition and cell death in response to high concentrations of estradiol. Collectively, these findings highlight the potential of new discoveries in sensitizing estrogen-sensitive tumors to chemotherapeutic drugs, and may lead to the development of new JNK-based effective therapies.
引用
收藏
页码:1281 / 1285
页数:5
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