Effect of endogenous TGF-beta1 and TNF-alpha on the As(2)O(3) inducing apoptosis of HL-60 cells.
- Author:
Yuan-zhong CHEN
1
;
Yong WU
;
Mei-juan HUANG
;
Lian-huang LU
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; Apoptosis; physiology; Arsenicals; pharmacology; Down-Regulation; HL-60 Cells; Humans; Oxides; pharmacology; Proto-Oncogene Proteins c-bcl-2; biosynthesis; genetics; RNA, Messenger; genetics; Receptors, Tumor Necrosis Factor; metabolism; Transforming Growth Factor beta1; biosynthesis; physiology; Tumor Necrosis Factor-alpha; physiology
- From: Chinese Journal of Hematology 2003;24(5):231-234
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of endogenous TGF-beta(1) and TNF-alpha on As(2)O(3) inducing apoptosis of HL-60 cells.
METHODSThe expressions of endogenous TGF-beta(1) and TNF-alpha in apoptotic HL-60 cells induced by As(2)O(3) were assayed by RT-PCR, quantitative RT-PCR, ELISA, DNA fragmentation and TUNEL. The effect of TGF-beta(1) and TNF-alpha antisense phosphorothioate oligodeoxynucleotides (PSODNs) on As(2)O(3) inducing apoptotic HL-60 cells was further studied.
RESULTS(1) Expressions of endogenous TGF-beta(1) and TNF-alpha were significantly up-regulated in As(2)O(3) inducing apoptotic HL-60 cells (from 13,546 +/- 124 and 497,216 +/- 187 before treatment to 23,273 +/- 229 and 674,217 +/- 189 after treatment, respectively), accompanied with down-regulated bcl-2 mRNA expression (from 10,424 +/- 274 before treatment to 3,361 +/- 89 after treatment). (2) TGF-beta(1) and TNF-alpha antisense PSODNs could rescue As(2)O(3) induced apoptosis of HL-60 cells, with a restoration of bcl-2 gene expression.
CONCLUSIONSEndogenous TGF-beta(1) and TNF-alpha played an important role in As(2)O(3) inducing HL-60 cells apoptosis through down-regulation of bcl-2 expression.
