Expression of heat-shock transcription factor 1 and X-linked inhibitor of apoptosis protein-associated factor-1 in gastrointestinal cancer.
- Author:
Ting LI
1
;
Cun-long CHEN
;
Ji-de WANG
;
Sheng-da CUI
;
Dan-yu CUI
;
Wen GUO
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line, Tumor; Colonic Neoplasms; genetics; metabolism; pathology; DNA-Binding Proteins; biosynthesis; genetics; Heat Shock Transcription Factors; Humans; Immunoblotting; Intracellular Signaling Peptides and Proteins; Neoplasm Proteins; biosynthesis; genetics; RNA Interference; Stomach Neoplasms; genetics; metabolism; pathology; Transcription Factors; biosynthesis; genetics; Transfection
- From: Journal of Southern Medical University 2008;28(3):487-490
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the expressions of X-linked inhibitor of apoptosis protein (XIAP)-associated factor-1 (XAFI) and heat-shock transcription factor 1 (HSF1) and their relationship in human gastrointestinal cancers.
METHODSImmunoblotting was used to analyze the expressions of HSF1 and XAF1 in gastric and colon cancer tissues and in gastrointestinal cancer cells. The gastrointestinal cancer cells were tranfected with a eukaryotic expression vector containing HSF1 gene fragment or subjected to RNA interference to induce up- or down-regulation of HSF1 expression, and the consequence changes in XAF1 expression in the cells was measured. XAF1 expression was also assayed in the cells after stress stimulation for HSF1 expression.
RESULTSThe expression of HSF1 was higher in gastrointestinal cancer tissues than in normal tissues. The expression of XAF1 and HSF1 was inversely correlated in the cancer cell lines, and stress stimuli of the cells up-regulated the expression of HSF1 but down-regulated XAF1 expression.
CONCLUSIONHSF1 expression is increased in gastrointestinal cancer tissues to result in suppressed expression of XAF1, which may be one of the reasons for the low expression of XAF1 in association with the defect of the apoptosis mechanisms in the cancer cells