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首页> 外文期刊>Archives of Toxicology >Tamoxifen-induced Ca2+ mobilization in bladder female transitional carcinoma cells.
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Tamoxifen-induced Ca2+ mobilization in bladder female transitional carcinoma cells.

机译：他莫昔芬诱导的Ca2 +动员在膀胱阴过渡癌细胞中。

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摘要

This study examined the effect of tamoxifen, an anti-breast cancer drug, on Ca2+ handling in bladder female transitional cancer cells. Changes in cytosolic free Ca2+ levels were recorded by using the Ca2+-sensitive dye fura-2. In a dose-dependent manner, tamoxifen induced intracellular free Ca2+ concentrations ([Ca2+]i) increases between 5 and 20 microM with an EC50 of 10 microM. External Ca2+ removal reduced the response by 60+/-6%. Addition of 3 mM Ca2+ caused a [Ca2+]i increase after pretreatment with 10 microM tamoxifen in Ca2+-free medium. In Ca2+-free medium, pretreatment with 10 microM tamoxifen abolished the [Ca2+]i increase induced by 1 microM thapsigargin, an endoplasmic reticulum Ca2+ pump inhibitor. Conversely, pretreatment with 1 microM thapsigargin prevented tamoxifen from releasing more Ca2+. Inhibition of phospholipase C-dependent inositol 1,4,5-tris-phosphate formation with 2 microM U73122 did not alter 10 microM tamoxifen-induced Ca2+ release. The [Ca2+]i increase induced by 5 microM tamoxifen was not altered by 10 microM La3+, nifedipine, verapamil, and diltiazem. Collectively, it was found that tamoxifen increased [Ca2+]i in bladder cancer cells by releasing Ca2+ from the endoplasmic reticulum Ca2+ stores in a manner independent of phospholipase C activity, and by inducing Ca2+ entry from external medium.
机译：本研究检测了Tamoxifen，抗乳腺癌药物，在膀胱雌性过渡癌细胞中Ca2 +处理的影响。通过使用Ca2 + - 敏感染料Fura-2记录细胞溶溶胶的变化。以剂量依赖性方式，诱导细胞内游离Ca 2 +浓度（[Ca2 +] I）增加5-20微米的EC50为10微米。外部CA2 +去除将响应减少60 +/- 6％。添加3mM Ca2 +导致[Ca2 +]在预处理中，在Ca2 + -Free培养基中的预处理后增加了[Ca2 +]。在Ca2 + -Free培养基中，用10μmOxifen的预处理废除了1微米尾，内质网Ca2 +泵抑制剂的[Ca2 +] I增加。相反，用1微米尾剂的预处理防止他莫昔芬释放更多CA2 +。抑制磷脂酶C依赖性肌醇1,4,5-三磷酸盐的形成，具有2微米U73122未改变10μmOxifen诱导的Ca2 +释放。由5微米毒素诱导的[Ca2 +]我增加未被10 microM La3 +，尼弗海内平，维拉帕米和Diltiazem改变。共同地发现，通过以与磷脂酶C活性的方式释放Ca2 +，通过释放Ca2 +，通过磷脂酶C活性的方式释放Ca 2+，并通过诱导外部培养基的Ca2 +进入，通过释放Ca2 +，在膀胱癌细胞中增加[Ca2 +] i。

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