Combination of pyrrolidine dithiocarbamate and paclitaxel suppresses proliferation and invasion of MDA-MB-231 cells

杨春蓉; 张徽; 黃伟; 刘琼

您当前的位置：

首页 >

文章列表页 >

Combination of pyrrolidine dithiocarbamate and paclitaxel suppresses proliferation and invasion of MDA-MB-231 cells

更新时间：2026-01-09

- Combination of pyrrolidine dithiocarbamate and paclitaxel suppresses proliferation and invasion of MDA-MB-231 cells
- Journal of Army Medical University Vol. 32, Issue 6, Pages: 576-579(2010)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：
  CLC： R730.23;R737.9;R979.1
- Published：2010
- 稿件说明：
移动端阅览
杨春蓉,张徽,黃伟,刘琼.PDTC联合紫杉醇降低MDA-MB-231细胞增殖侵袭能力[J].陆军军医大学学报(原第三军医大学学报),2010,32(06):576-579.

　Yang Chunrong,Zhang Hui,Huang Wei,Liu Qiong.Combination of pyrrolidine dithiocarbamate and paclitaxel suppresses proliferation and invasion of MDA-MB-231 cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(06):576-579.
杨春蓉,张徽,黃伟,刘琼.PDTC联合紫杉醇降低MDA-MB-231细胞增殖侵袭能力[J].陆军军医大学学报(原第三军医大学学报),2010,32(06):576-579. DOI：

　Yang Chunrong,Zhang Hui,Huang Wei,Liu Qiong.Combination of pyrrolidine dithiocarbamate and paclitaxel suppresses proliferation and invasion of MDA-MB-231 cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(06):576-579. DOI：

摘要

目的探讨核因子-κB(NF-κB)抑制剂——吡咯烷二硫代氨基甲酸盐(pyrrolidine dithiocarbamate，PDTC)联合紫杉醇(Paclitaxel)对人乳腺癌MDA-MB-231细胞增殖侵袭能力的影响。方法 MTT及FCM法测定细胞增殖和周期变化，RT-PCR检测细胞NF-κB p65 mRNA的变化，Western blot检测细胞NF-κB p65、MMP-9及TIMP-1蛋白表达变化，侵袭、迁移和黏附实验测定细胞侵袭转移能力的改变。结果 PDTC联合紫杉醇能明显抑制肿瘤细胞生长(P0.05)，细胞周期阻滞在G

期，并可抵消紫杉醇对NF-κB的激活，使NF-κB p65 mRNA及蛋白的表达均降低(P0.05)。PDTC降低MDA-MB-231细胞的侵袭转移能力，与紫杉醇联合应用后作用增强(P0.01)。结论 PDTC联合紫杉醇能降低乳腺癌MDA-MB-231细胞的侵袭转移能力，其机制可能与PDTC抑制NF-κB的表达相关。

Abstract

Objective To investigate the effect of the nuclear factor-κB (NF-κB) inhibitor

pyrrolidine dithiocarbamate (PDTC) and paclitaxel on the proliferation and invasion of human breast cancer cell line MDA-MB-231. Methods The MDA-MB-231 cells were treated with PDTC (100 μmol/L) or paclitaxel (1 μmol/L)

or combined treatment. The effect of proliferation was analyzed by MTT assay. The cell cycle was evaluated by flow cytometry. RT-PCR was used to detect the expression of NF-κB p65 mRNA. Western blotting were used to determing the expression of NF-κB p65

MMP-9 and TIMP-1 i

n MDA-MB-231 cells after treatment. The invasion ability of MDA-MB-231 cells was tested ty the invasion

migration and cell adhesion assay. Results The cell growth was significantly slowed down and the cell cycle was arrested at G

phase after combined treatment. The expression of NF-κB p65 and MMP-9 was downregulated (P0.05) compared with paclitaxel treatment group

and the invasion ability of MDA-MB-231 cells was decreased after combined treatment (P0.01). Conclusion PDTC combined with paclitaxel effectively inhibits cell proliferation

induces cell cycle arrest

and decreases cell invasion ability of human breast cancer MDA-MB-231 cells. Its mechanism may be associated with PDTC inhibiting the NF-κB-related gene expression.

关键词

Keywords

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Effects of over-expression of Bmi-1 on invasion and metastasis in human mammary carcinoma cell line BT474

Effect of siRNA mediated down-regulation of AnnexinⅡ on human breast cancer cell line MDA-MB-435S

A novel estrogen receptor expression stratification (low/moderate/high) based on Chinese population provides more accurate prognosis prediction for HR⁺/HER2^- early breast cancer patients

Celastrol attenuates sodium oxalate-induced acute kidney injury and crystal deposition by inhibiting NF-κB

Downregulating RRM2B expression to increase radiation sensitivity of breast cancer cells

Related Author

李海玉

宋方洲

卜友泉

易发平

朱慧芳

汪长

刘革力

武向梅

Related Institution

Department of Breast and Thyroid Surgery， First Affiliated Hospital， Army Medical University （Third Military Medical University）

Urinary Nephropathy Center， the Second Affiliated Hospital of Chongqing Medical University

Department of Immunology， College of Basic Medical Sciences

Department of Nephrology and Urology， No. Hospital958， First Affiliated Hospital， Army Medical University （Third Military Medical University）

⁰