ArticleExperimental and therapeutic medicine2010
G2/M accumulation in prostate cancer cell line PC-3 is induced by Cdc25 inhibitor 7-chloro-6-(2-morpholin-4-ylethylamino) quinoline-5, 8-dione (DA 3003-2).
Article in Experimental and therapeutic medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Synthesis and Study of Substituted Chalcones Combined with Fluoroazobenzenes-New Photoswitches for Application in Biological Systems.Molecules (Basel, Switzerland) · 2026Article
- Phosphatases and kinases regulating CDC25 activity in the cell cycle: clinical implications of CDC25 overexpression and potential treatment strategies.Molecular and cellular biochemistry · 2016Review
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1 author at 1 institution in 1 country.
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Abstract
Cdc25 phosphatases are dual-specific phosphatases that play a role in cell cycle progression. In many human cancers, Cdc25 phosphatases are overexpressed as compared with normal tissues. In addition, overexpression of Cdc25 phosphatases in prostate cancer is correlated with disease progression. The antiproliferative efficacy of Cdc25 phosphatase inhibitor 7-chloro-6-(2-morpholin-4-ylethylamino) quinoline-5, 8-dione (DA 3003-2) was investigated in the PC-3 asynchronous human prostate cancer cell line using a cell-based assay. The time course changes in cell cycle distribution and the modulation of cell cycle regulators after DA 3003-2 administration were analyzed using the MTT assay. We found that the relative IC(50) of DA 3003-2 was 2-fold lower as compared with its congener (2-mercaptoethanol)-3-methyl-1, 4-naphthoquinone (NSC 672121). Asynchronous PC-3 cells accumulated in the G2/M phase at 24 h after treatment with 10 μM DA 3003-2 or 20 μM NSC 672121, which represent IC(70) concentrations. Treatment of cells with DA 3003-2 caused hyperphosphorylation of Cdc2 tyr(15) in cyclin B(1) and cyclin A complexes. DA 3003-2 did not downregulate the protein expression levels of Cdc25s, cyclins and cyclin-dependent kinases (Cdks). To conclude, after DA 3003-2 administration asynchronous PC-3 cells accumulated in the G2/M phase, with hyperphosphorylation of the G2/M cyclin-Cdk complex.
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