The effect of cell killing and apoptosis by human herpes simplex virus- thymidine kinase/ganciclovir system combined with allitride in BIU87 cells.
- Author:
Shao-peng QIU
1
;
Xiao-peng MAO
;
Kai-yuan CAO
;
Xian-jing CHEN
;
Guang-qing YUAN
;
Lin XU
;
Xiao-rong HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Drug Synergism; Ganciclovir; pharmacology; Genetic Therapy; Herpesvirus 1, Human; enzymology; genetics; Humans; In Vitro Techniques; Sulfinic Acids; pharmacology; Thymidine Kinase; genetics; Transfection; Urinary Bladder Neoplasms; pathology; therapy
- From: Chinese Journal of Surgery 2005;43(6):382-386
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the killing effect of human herpes simplex virus-thymidine kinase/ganciclovir (HSV-TK/GCV) system combined with allitride and the possible apoptosis mechanism in BIU87 cells.
METHODSThe cytotoxicity after combination were estimated by theamine blue tetrazolium bromide (MTT). The morphological changes were observed with inverted microscope and in-situ cell apoptosis detection kit. Changes of apoptosis rate and cell cycle were assessed by flow cytometry. B-cell lymphoma-2 (bcl-2), bax, caspase-3 (cysteine aspartate specific proteinase) mRNA changes were detected by reverse transcriptase polymerase chain reaction, and caspase-3 activity was estimated with colorimetry.
RESULTSFor combination group, the cell killing rate was raised to 72.50% to compare with 35.00% of GCV and 37.00% of allitride separately and there was a synergistic effect between these two drugs. The cell apoptosis was induced in all three groups and for the combination group the time of S-phase and G(2)-phase arrest were earlier than other two groups. Both drugs could inhibit the expression of bcl-2 and promote the expression and activity of caspase-3.
CONCLUSIONSThe combination of HSV-TK/GCV system with allitride can inhibit the proliferation of BIU87 cells congenerously through apoptosis, which may be correlated with S- and G(2)-phase arrest, down-regulation of bcl-2 and increased caspase-3 expression and its activity.