1,25-dihydroxyvitamin D<sub>3</sub> induces cell cycle arrest of MDA-MB-231 cells transfected with exogenous ERα expression vector containing vitamin D response elements

郎海滨; 糜漫天

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1,25-dihydroxyvitamin D₃ induces cell cycle arrest of MDA-MB-231 cells transfected with exogenous ERα expression vector containing vitamin D response elements

更新时间：2026-01-09

- 1,25-dihydroxyvitamin D₃ induces cell cycle arrest of MDA-MB-231 cells transfected with exogenous ERα expression vector containing vitamin D response elements
- Journal of Army Medical University Vol. 30, Issue 22, Pages: 2086-2089(2008)
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  CLC： R329.28;R737.9;R966
- Published：2008
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郎海滨,糜漫天.1,25二羟维生素D3靶控VDRE-ERα表达载体对MDA-MB-231细胞周期的影响[J].陆军军医大学学报(原第三军医大学学报),2008,30(22):2086-2089.

　LANG Hai-bin,MI Man-tian.1,25-dihydroxyvitamin D3 induces cell cycle arrest of MDA-MB-231 cells transfected with exogenous ERα expression vector containing vitamin D response elements[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(22):2086-2089.
郎海滨,糜漫天.1,25二羟维生素D3靶控VDRE-ERα表达载体对MDA-MB-231细胞周期的影响[J].陆军军医大学学报(原第三军医大学学报),2008,30(22):2086-2089. DOI：

　LANG Hai-bin,MI Man-tian.1,25-dihydroxyvitamin D3 induces cell cycle arrest of MDA-MB-231 cells transfected with exogenous ERα expression vector containing vitamin D response elements[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(22):2086-2089. DOI：

摘要

目的探讨1，25二羟维生素D

靶控的雌激素受体α表达载体（VDRE-Tk-ERα）对雌激素受体阴性的MDA-MB-231乳腺癌细胞周期进程的影响及其机制。方法利用MTT法检测1，25二羟维生素D

联合他莫西芬对转染VDRE-Tk-ERα表达载体的MDA-MB-231细胞增殖能力的影响，通过流式细胞仪法检测1，25二羟维生素D

联合他莫西芬对转染该表达质粒的MDA-MB-231细胞周期相的分布。用RT-PCR、Western blot和免疫沉淀法检测细胞Rb及其磷酸化水平、Cyclin D

、CDK

的表达以及Cyclin D

/CDK

激酶复合物的结合力变化。结果 1，25二羟维生素D

联合他莫西芬能够有效抑制转染该质粒的MDA-MB-231细胞的增殖活性并将其细胞周期进程阻遏于G

期。与此同时，Cyclin D

的表达则显著降低，其与CDK

的结合力亦显著降低。Rb的表达虽无显著变化，但其磷酸化水平显著下降。结论 1，25二羟维生素D

可通过靶控MDA-MB-231细胞内外源性雌激素受体α的表达进而对G

/S期相关分子的表达和活性进行调控从而阻止雌激素受体α阴性的乳腺癌细胞的周期进程并恢复对他莫西芬的化疗敏感性。

Abstract

Objective To investigate the effects and molecular mechanism of tamoxifen on cell cycle distribution of ER-negative MDA-MB-231 cells re-expressing exogenous ERα gene under induction of Vit D

. Methods ERα/pcDNA3.1+ eukaryotic plasmid containing 4 copies of vitamin

D response elements (VDRE) and Tk promoter was transfected into MDA-MB-231 cells. MTT assay and flow cytometry were used to analyze the inhibitory effects of Vit D

and Tamoxifen on cell proliferation and cell cycle distribution. Then RT-PCR and Western blot assay were employed to detect the expressions of Cyclin D

CDK

Rb and phosphorylated Rb. The binding affinity of Cyclin D

/CDK

complex was also analyzed by using immunoprecipitation assay. Results After concomitant treatment with Vit D

and Tamoxifen for 72 h

Vit D

and Tamoxifen synergetically inhibited proliferation of MDA-MB-231

VDRE-ERα

cells

and the majority of cells were arrested in G

phase. Cyclin D

expression and the binding affinity of Cyclin D

/CDK

complex were markedly down-regulated after 24 h of the concomitant treatment. Concurrently

the phosphorylation of Rb protein was also effectively inhibited while its expression exhibited no evident changes. Conclusion Vit D

could effectively restore the sensitivity of ER-negative breast cancer cells transfected with exogenous ERα vector containing VDREs-Tk promoter to Tamoxifen by regulating the expression and activity of G

/S phase-related molecules.

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1,25-dihydroxyvitamin D3 induces cell cycle arrest of MDA-MB-231 cells transfected with exogenous ERα expression vector containing vitamin D response elements

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摘要

Abstract

关键词

Keywords

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1,25-dihydroxyvitamin D₃ induces cell cycle arrest of MDA-MB-231 cells transfected with exogenous ERα expression vector containing vitamin D response elements