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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2002-6-13
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pubmed:abstractText |
Prostate cancer is the most commonly diagnosed cancer and the second leading cause of cancer related deaths in men in the United States. Ciprofloxacin is a relatively non-toxic antibiotic that can be easily administered orally with large volume of distribution and good tissue penetration. Studies from others and our laboratory have recently reported its anti-tumor activity in a variety of human tumor cells. In our current experiment, we studied the effect of ciprofloxacin on a hormone resistant prostate cancer (HRPC) cell line, PC-3. Our study shows significant in vitro cell growth inhibition of PC-3 cell line (p=0.0001) and also shows that there is a synergistic increase in the antiproliferative effect of etoposide when these cells are pretreated with ciprofloxacin for 24 h, prior to etoposide exposure (p=0.0001). Western blot analysis of the protein extracts from these cells showed down-regulation of Bcl-2, altering the ratio of Bax:Bcl-2 favoring apoptosis. In our study no significant effect was seen on p21WAF1 expression by the combination of ciprofloxacin and etoposide but there was down-regulation of p21WAF1 gene by ciprofloxacin alone. Ciprofloxacin also inhibited NF-kappaB binding to DNA. Further studies in this area are warranted as the roles of p21WAF1, Bax/Bcl-2 and NF-kappaB may be important molecular events in mediating the antiproliferative and apoptosis inducing effect of etoposide in combination with ciprofloxacin in HRPC cells.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Infective Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents, Phytogenic,
http://linkedlifedata.com/resource/pubmed/chemical/BAX protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CDKN1A protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ciprofloxacin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase Inhibitor...,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclins,
http://linkedlifedata.com/resource/pubmed/chemical/Etoposide,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1019-6439
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
207-11
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12063570-Anti-Infective Agents,
pubmed-meshheading:12063570-Antineoplastic Agents, Phytogenic,
pubmed-meshheading:12063570-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:12063570-Apoptosis,
pubmed-meshheading:12063570-Cell Division,
pubmed-meshheading:12063570-Ciprofloxacin,
pubmed-meshheading:12063570-Cyclin-Dependent Kinase Inhibitor p21,
pubmed-meshheading:12063570-Cyclins,
pubmed-meshheading:12063570-Down-Regulation,
pubmed-meshheading:12063570-Drug Synergism,
pubmed-meshheading:12063570-Electrophoretic Mobility Shift Assay,
pubmed-meshheading:12063570-Etoposide,
pubmed-meshheading:12063570-Gene Expression Regulation,
pubmed-meshheading:12063570-Humans,
pubmed-meshheading:12063570-Male,
pubmed-meshheading:12063570-Middle Aged,
pubmed-meshheading:12063570-NF-kappa B,
pubmed-meshheading:12063570-Prostatic Neoplasms,
pubmed-meshheading:12063570-Proto-Oncogene Proteins,
pubmed-meshheading:12063570-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:12063570-Radiation Tolerance,
pubmed-meshheading:12063570-Tumor Cells, Cultured,
pubmed-meshheading:12063570-bcl-2-Associated X Protein
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pubmed:year |
2002
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pubmed:articleTitle |
Ciprofloxacin inhibits cell growth and synergises the effect of etoposide in hormone resistant prostate cancer cells.
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pubmed:affiliation |
Department of Hematology/Oncology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI 48201, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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