Anion exchanger inhibitor DIDS induces human poorly-differentiated malignant hepatocellular carcinoma HA22T cell apoptosis.

中山醫學大學機構典藏 CSMUIR > 醫學院 > 生化微生物免疫研究所 > 期刊論文 > Item 310902500/11479

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11479

Title:	Anion exchanger inhibitor DIDS induces human poorly-differentiated malignant hepatocellular carcinoma HA22T cell apoptosis.
Authors:	Liu, CJ Hwang, JM Wu, TT Hsieh, YH Wu, CC Hsieh, YS Tsai, CH Wu, HC Huang, CY Liu, JY
Contributors:	中山醫學大學
Keywords:	HA22T hepatocellular carcinoma cells;Anion exchanger 2;DIDS;Apoptosis Proliferation;Anion transport activity
Date:	2008
Issue Date:	2015-07-21T09:09:27Z (UTC)
ISSN:	0300-8177
Abstract:	Anion exchangers (AEs) of the Cl(-)/HCO3(-) exchanger family contribute to the regulation of intracellular acid-base balance. Recently, we found that anion exchanger 2 (AE2) was significantly expressed in human hepatocellular carcinoma (HCC) and in poorly-differentiated human HCC HA22T/VGH cells. In the present study, we further explored the pharmacological function of AE in four human HCC cell lines (SK-Hep-1, HA22T/VGH, HepG2, and Hep3B) following the treatment of 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), an AEs specific inhibitor. After administrations with 400-1000 microM of DIDS, cell proliferation was greatly inhibited in a dose-dependent manner from 47.5 to 65.0% in higher malignant HA22T/VGH cells, but not in other cell lines. The results of 4,6-diamidino-2-phenylindole (DAPI) staining, DNA fragmentation and flow cytometric analysis further revealed that cell apoptosis induced by DIDS was also observed in HA22T/VGH cells. Therefore, these findings suggested that AE may be involved, in part, in the proliferation and survival of HA22T cells and could be a new potential therapeutic target against specific human HCC.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11479
Relation:	Mol Cell Biochem. 2008 Jan;308(1-2):117-25.
Appears in Collections:	[生化微生物免疫研究所] 期刊論文

Files in This Item:

File	Description	Size	Format
index.html	期刊論文	0Kb	HTML	350	View/Open

View Licence

Loading...