Up-expression of IL-6 and down-expression of TNFalpha may be involved in the regulation of apoptosis induced by antisense bcl-2 oligodeoxynucleotides.
- Author:
Xinji CHEN
1
;
Jianda HU
;
Zhizhe CHEN
;
Lianhuang LU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; genetics; Chemotactic Factors; genetics; Gene Expression Regulation, Neoplastic; drug effects; Humans; In Situ Nick-End Labeling; Inhibitor of Apoptosis Proteins; Interleukin-6; genetics; Microtubule-Associated Proteins; genetics; Neoplasm Proteins; Oligonucleotides, Antisense; pharmacology; Proto-Oncogene Proteins; genetics; Proto-Oncogene Proteins c-bcl-2; genetics; Proto-Oncogene Proteins c-myc; genetics; RNA, Messenger; drug effects; genetics; metabolism; S100 Proteins; genetics; Transforming Growth Factor beta; genetics; Transforming Growth Factor beta1; Tumor Cells, Cultured; drug effects; Tumor Necrosis Factor-alpha; genetics; bcl-2-Associated X Protein
- From: Chinese Journal of Medical Genetics 2002;19(6):495-498
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the regulation mechanism of apoptosis induced by the antisense bcl-2 treatment.
METHODSDNA content analysis and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) were adopted to detect apoptosis. Semi-quantitative reverse transcription-PCR was performed to detect the mRNA expression of bcl-2 c-myc survivin bax s100A(2) TNFalpha TGFbeta(1) and IL-6 in the small-cell lung cancer cell line NCI-H446 treated with antisense bcl-2 oligodeoxynucliotide.
RESULTSbcl-2 AS-PS-ODN treatment could induce apoptosis, accompanied with 72.71% up-regulation of IL-6 and 65.90% down-regulation of TNFalpha, whereas little or no effect was seen on c-myc survivin bax s100A(2) and TGFbeta(1).
CONCLUSIONIL-6 and TNFalpha may be involved in the regulation of apoptosis induced by antisense bcl-2 treatment.
