Abstract | OBJECTIVE: METHODS: The cell proliferation, cell cycle, and apoptosis were measured in Ishikawa endometrial cancer cells after PsA treatment. RESULTS: PsA significantly inhibited the proliferation of Ishikawa cells in a dose-dependent manner. PsA markedly induced the expression of acetylated H3 and H4 histone proteins. In addition, PsA markedly up-regulated the expression of cyclin-dependent kinase inhibitor, p21(WAF1), and down-regulated the expression of pRb, cyclins, and CDKs, which lead to induce cell cycle arrest. Cell cycle analysis indicated that PsA treatment increased the proportion of cells in the G0/G1 and G2/M phases, and decreased the ratio of cells in the S phase. CONCLUSION: The PsA treatment resulted in the significant induction of apoptosis, which was associated with p53 independent p21(WAF1) expression. These results suggest that PsA exhibits the antiproliferative effects on endometrial cancer cells through selective induction of genes related to cell cycle arrest and apoptosis.
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Authors | Mee Young Ahn, Jee H Jung, Yong Jin Na, Hyung Sik Kim |
Journal | Gynecologic oncology
(Gynecol Oncol)
Vol. 108
Issue 1
Pg. 27-33
(Jan 2008)
ISSN: 1095-6859 [Electronic] United States |
PMID | 17920664
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents
- Cell Cycle Proteins
- Disulfides
- Enzyme Inhibitors
- Histone Deacetylase Inhibitors
- Histones
- psammaplin A
- Tyrosine
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Topics |
- Acetylation
(drug effects)
- Antineoplastic Agents
(pharmacology)
- Apoptosis
(drug effects)
- Cell Cycle
(drug effects)
- Cell Cycle Proteins
(biosynthesis)
- Cell Line, Tumor
- Disulfides
(pharmacology)
- Dose-Response Relationship, Drug
- Endometrial Neoplasms
(drug therapy, enzymology, pathology)
- Enzyme Inhibitors
(pharmacology)
- Female
- Histone Deacetylase Inhibitors
- Histones
(metabolism)
- Humans
- Tyrosine
(analogs & derivatives, pharmacology)
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