Effects of Polyamines on TNFalpha- or Tamoxifen-induced Apoptosis in Human Breast Cancer Cells.
- Author:
Ji Young KIM
1
;
Ki Young KIM
;
Kyeong Hee LEE
;
Ki Whan HONG
;
Byeong Gee KIM
Author Information
1. Division of Biological Sciences, College of Natural Sciences, Korea. bgkim@pnu.edu
- Publication Type:Original Article
- Keywords:
Polyamines;
Apoptosis;
TNFalpha;
Tamoxifen
- MeSH:
Antioxidants;
Apoptosis*;
Breast Neoplasms*;
Breast*;
Cell Death;
Cell Survival;
DNA Fragmentation;
Electrophoresis, Agar Gel;
Estrogens;
Fluorescence;
Humans*;
MCF-7 Cells;
Polyamines*;
Reactive Oxygen Species;
Spermine;
Tamoxifen;
Tumor Necrosis Factor-alpha
- From:Cancer Research and Treatment
2001;33(5):385-391
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: To investigate the effects of polyamines on tumor necrosis factor alpha (TNFalpha)-or tamoxifen (TAM)-induced apoptosis in estrogen receptor (ER)-positive MCF- 7 and ER-negative MDA-MB-231 human breast cancer cells. MATERIALS AND METHODS: Cell viability was assessed by using MTT assay. Reactive oxygen species (ROS) generation was measured using 2', 7'-dichlorofluorescin diacetste (DCFDA) by fluorescence plate reader. DNA fragmentation was assessed by 1.5% agarose gel electrophoresis. RESULTS: TNFalpah and TAM showed significant dose- and time- dependent inhibitory effects on the growth of MCF-7 human cells. However, the growth of MDA-MB-231 cells were not inhibited by TNFalpha or TAM treatment. The generation of ROS was increased in dose-and time-dependent manner by TNFalpha treatment in MCF-7 cells. Polyamines, especially spermine suppressed TNFalpha-induced ROS generation in MCF-7 cells. Antioxidant effects of polyamines were also demonstrated by DNA fragmentation, cell morphology as well as ROS generation assay. Polyamines also blocked TAM-induced cell death in MCF-7 cell. However, MDA-MB-231 cells showed resistance to the cytotoxic effects of TNFalpha or TAM. CONCLUSION: These results suggest that polyamines may prevent TNFalpha or TAM-induced apoptosis in MCF-7 human breast cancer cells.
