Intrinsic apoptotic and thioredoxin pathways in human prostate cancer cell response to histone deacetylase inhibitor

Xu  WS; Ngo  L; Perez  GDokmanovic  MMarks  PA

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Intrinsic apoptotic and thioredoxin pathways in human prostate cancer cell response to histone deacetylase inhibitor

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There is a great need to develop better mechanism-based therapies for prostate cancer. In this investigation, we studied four human prostate cancer cell lines, LNCaP, DU145, LAPC4, and PC3, which differ in response to the histone deacetylase inhibitor, suberoylanilide hydroxamic acid (vorinostat), a new anticancer drug. Examining the role of intrinsic mitochondrial caspase-dependent apoptosis and caspase-independent, reactive oxygen species (ROS) facilitated cell death, has provided an understanding of mechanisms that may determine the varied response to the histone deacetylase inhibitor. We found striking differences among these cancer cells in constitutive expression and response to suberoylanilide hydroxamic acid in levels of antiapoptotic and proapoptotic proteins, mitochondria membrane integrity, activation of caspases, ROS accumulation, and expression of thioredoxin, the major scavenger of ROS. Identifying these differences can have predictive value in assessing therapeutic response and identifying targets to enhance therapeutic efficacy.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2006年第42期|15540-15545|共6页
作者
Xu WS; Ngo L; Perez GDokmanovic MMarks PA;
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作者单位

Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
mitochondria membrane; reactive oxygen species; suberoylanilide hydroxamic acid; thioredoxin-binding protein; caspase; SUBEROYLANILIDE HYDROXAMIC ACID; UP-REGULATED PROTEIN-1; NEGATIVE REGULATOR; GENE-EXPRESSION; LEUKEMIA-CELLS; TUMOR-CELLS; GROWTH; DEATH; IDENTIFICATION; ACTIVATION;

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Intrinsic apoptotic and thioredoxin pathways in human prostate cancer cell response to histone deacetylase inhibitor

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