Effect of FGF-2 on survivin and subcellular location of Smac in human small cell lung cancer cell NCI-H446.
- Author:
De-sheng XIAO
1
;
Hui-qiu CAO
;
Zheng-hao DENG
;
Xiao-hui QU
;
Ji-fang WEN
;
Jian-hua ZHOU
;
Chun-yan FU
Author Information
1. Department of Pathology, Xiangya School of Medicine, Central South University, Changsha 410078, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Apoptosis Regulatory Proteins;
Cytoplasm;
metabolism;
Fibroblast Growth Factor 2;
pharmacology;
Humans;
Inhibitor of Apoptosis Proteins;
Intracellular Signaling Peptides and Proteins;
metabolism;
Lung Neoplasms;
metabolism;
pathology;
Microtubule-Associated Proteins;
biosynthesis;
Mitochondria;
metabolism;
Mitochondrial Proteins;
metabolism;
Small Cell Lung Carcinoma;
metabolism;
pathology;
Survivin;
Tumor Cells, Cultured
- From:
Journal of Central South University(Medical Sciences)
2008;33(8):705-711
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of basic fibroblast growth factor (FGF-2)on survivin and subcellular location of Smac in human small cell lung cancer (SCLC) cell NCI-H446.
METHODS:Western blot was used to detect the expression of survivin protein induced by FGF-2. The release of Smac from mitochondria to cytoplasm affected by FGF-2 was observed by Western blot and immunofluorescence. Apoptosis of NCI-H446 cells was detected with flow cytometry and Hoechst 33258 staining.
RESULTS:The expression of survivin could be up-regulated in response to FGF-2 treatment in NCI-H446 cells, and the level of survivin expression is related to the concentration and time of FGF-2 treatment. FGF-2 could inhibit the release of Smac from the mitochondria to cytoplasm induced by serum starving. FGF-2 could inhibit the apoptosis induced by serum starving.
CONCLUSION:FGF-2 up-regulates the expression of survivin protein in NCI-H446 cells, and blocks the release of Smac from mitochondria cytoplasm. Survivin and Smac might play important roles in the apoptosis inhibited by FGF-2.
