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针对病种:乳腺癌

发表时间:2011年1月

发表国家:希腊

登载刊物:抗癌研究

研究单位:美国芝加哥德保罗大学生物科学学院和护理学院

研究人员:约翰 格温等

主要结论:高、 低浓度的染料木黄酮诱导 p90RSK 磷酸化 中ERK1/2-独立性的减少。在接触染料木黄酮48 小时后这种效应伴随着高浓度时细胞增殖降低而低浓度时响应增强。染料木黄酮在 T47D 细胞中的浓度依赖性活性可能是由于微信号分子的差异活性.

Anticancer Research, 2011, 31(1):209-14.

Effect of Genistein on p90RSK Phosphorylation and Cell Proliferation in T47D Breast Cancer Cells

John Gwin, et al

Department of Biological Sciences and Nursing, DePaul University, Chicago, IL 60614, USA.

BACKGROUND: The molecular mechanisms of genistein's proliferative effects on breast cancer cells are largely unknown. This study aimed to examine estrogen-receptor (ER)-related signaling molecules involved in genistein-associated cell proliferation and survival (ERK1/2, p90RSK, JNK, Akt and NFκB) and to correlate these results to cell proliferation.

MATERIALS AND METHODS: The effect of genistein on cell-signaling molecules was determined in T47D breast cancer cells by a Bioplex phosphoprotein detection kit. These results were confirmed by Western blotting and were correlated to cell proliferation by MTT assay.

RESULTS: Low and high concentrations of genistein induced an ERK1/2-independent decrease in phosphorylated p90RSK. This effect was accompanied by decreased cell proliferation at high concentrations and an increased response at low concentrations of genistein following a 48-hour exposure.

CONCLUSION: Concentration-dependent actions of genistein in T47D cells may be due to differential activation of signaling molecules.


希腊《抗癌研究》,
20111

T47D 乳腺癌细胞中金雀异黄素对 p90RSK 磷酸化和细胞增殖的影响

约翰  格温等

美国芝加哥德保罗大学生物科学学院和护理学院

背景︰ 金雀异黄素对乳腺癌细胞增殖作用的分子机制是未知的。本研究旨在探讨雌激素受体 (ER)-相关信号分子参与金雀异黄素相关细胞增殖和生存 ERK1/2p90RSKJNK Akt NFκB ,并且将这些结果与细胞增殖联系起来。

材料和方法︰通过Bioplex 磷蛋白检测试剂盒确认金雀异黄素对T47D 乳腺肿瘤细胞信号转导分子的影响。这些结果被免疫印迹法证实并且MTT 法检测证明与细胞增殖相关。

结果︰ 高、 低浓度的染料木黄酮诱导 p90RSK 磷酸化 ERK1/2-独立性的减少。在接触染料木黄酮48 小时后这种效应伴随着高浓度时细胞增殖降低而低浓度时响应增强。

结论︰ 染料木黄酮在 T47D 细胞中的浓度依赖性活性可能是由于微信号分子的差异活性。

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