Lactacystin augments the sulindac-induced apoptosis in HT-29 cells

被引：15

作者：

Choi, HJ

Kim, HH

Lee, HS

Huh, GY

Seo, SY

Jeong, JH

Kim, JM

Yoo, YH ^{[1
]}

机构：

[1] Dong A Univ Coll Med, Dept Anat & Cell Biol, Pusan 602714, South Korea

[2] Dong A Univ Coll Med, Dept Gen Surg, Pusan 602714, South Korea

[3] Dong A Univ Coll Med, Dept Radiat Oncol, Pusan 602714, South Korea

[4] Dong A Univ Coll Med, Dept Pathol, Pusan 602714, South Korea

[5] Dong A Univ Coll Med, Dept Microbiol & Immunol, Pusan 602714, South Korea

来源：

APOPTOSIS | 2003年 / 8卷 / 03期

关键词：

apoptosis; colon cancer; lactacystin; proteasome; sulindac;

D O I：

10.1023/A:1023681007766

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The present study was conducted to explore the potential role of proteasome pathway in NSAIDs-induced apoptosis. We employed sulindac as a NSAID, and chose the lactacystin for inhibition of proteasome activity. Assessment of apoptosis and proteasome activity assay were undertaken. We demonstrated that sulindac treatment resulted in a decrease of proteasome activity, and that the co-treatment of a proteasome inhibitor lactacystin potentiated the extent of sulindac-induced apoptosis in HT-29 cells by augmentation of the decrease in proteasome activity. Elucidation of the mechanism underlying the regression of colon cancers by combinations of sulindac and lactacystin seems to be an immediate challenge for the near future.

引用

页码：301 / 305

页数：5

共 20 条

[1]

Adams J, 1999, CANCER RES, V59, P2615

[2] Proteasome inhibitors induce apoptosis in glucocorticoid-resistant chronic lymphocytic leukemic lymphocytes [J].