Inhibitory effects of transfected Bcl-XL antisense oligodeoxynucleotide on proliferation of esophageal cancer cells and growth of human esophageal carcinoma in nude mice.
- Author:
Lei ZHANG
1
;
Hong-tao WEN
;
Lan ZHANG
;
Kui-sheng CHEN
;
Yun-han ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Esophageal Neoplasms; metabolism; pathology; Female; Humans; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Transplantation; Oligodeoxyribonucleotides, Antisense; pharmacology; RNA, Messenger; biosynthesis; genetics; Transfection; bcl-X Protein; biosynthesis; genetics
- From: Chinese Journal of Pathology 2005;34(7):402-406
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the biologic effects of Bcl-XL antisense oligodeoxynucleotide (ASODN) transfected into cultured esophageal carcinoma cells and human esophageal carcinoma xenograft in nude mice.
METHODSCationic liposome-mediated ASODN was used to transfect esophageal carcinoma cells. RT-PCR, Western blot, MTT assay, flow cytometry and in-situ apoptosis cells detection (TUNEL detection) were used to systematically study the biological effects of the transfected cells in vitro and in vivo.
RESULTSMTT assay showed that the proliferation of esophageal carcinoma cells in the ASODN group decreased significantly as compared with control (P < 0.05), along with a 57.3% inhibitory rate of Bcl-XL mRNA, a significant decrease of Bcl-XL protein and the apoptosis rates of (31.1 +/- 5.8)% and 35.0% by flow cytometry and TUNEL assay, respectively (P < 0.01, as compared with controls). The growth of human esophageal carcinoma in nude mice was also significantly inhibited in the ASODN group (P < 0.05), along with a significant decrease of Bcl-XL mRNA and protein expression, and also an enhanced apoptosis of the tumor cells in nude mice.
CONCLUSIONSBcl-XL ASODN can effectively inhibit the proliferation of esophageal carcinoma cells in vitro and the growth of the tumor in vivo. The suppression of Bcl-XL expression by ASODN may offer both a therapeutic approach and an important theoretic foundation for gene therapy against esophageal carcinoma.