Antiproliferative effects of carbon monoxide on pancreatic cancer
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
24433995
DOI
10.1016/j.dld.2013.12.007
PII: S1590-8658(13)00695-6
Knihovny.cz E-zdroje
- Klíčová slova
- Anticancer effects, Heme catabolic pathway, Heme oxygenase,
- MeSH
- duktální karcinom pankreatu * MeSH
- fosforylace účinky léků MeSH
- gasotransmitery farmakologie MeSH
- lidé MeSH
- myši nahé MeSH
- myši MeSH
- nádory slinivky břišní * MeSH
- organokovové sloučeniny farmakologie MeSH
- oxid uhelnatý farmakologie MeSH
- proliferace buněk účinky léků MeSH
- protoonkogenní proteiny c-akt účinky léků metabolismus MeSH
- xenogenní modely - testy antitumorózní aktivity MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- gasotransmitery MeSH
- organokovové sloučeniny MeSH
- oxid uhelnatý MeSH
- protoonkogenní proteiny c-akt MeSH
- tricarbonyldichlororuthenium (II) dimer MeSH Prohlížeč
BACKGROUND: Carbon monoxide, the gaseous product of heme oxygenase, is a signalling molecule with a broad spectrum of biological activities. The aim of this study was to investigate the effects of carbon monoxide on proliferation of human pancreatic cancer. METHODS: In vitro studies were performed on human pancreatic cancer cells (CAPAN-2, BxPc3, and PaTu-8902) treated with a carbon monoxide-releasing molecule or its inactive counterpart, or exposed to carbon monoxide gas (500 ppm/24h). For in vivo studies, pancreatic cancer cells (CAPAN-2/PaTu-8902) were xenotransplanted subcutaneously into athymic mice, subsequently treated with carbon monoxide-releasing molecule (35 mg/kg b.w. i.p./day), or exposed to safe doses of carbon monoxide (500 ppm 1h/day; n = 6 in each group). RESULTS: Both carbon monoxide-releasing molecule and carbon monoxide exposure significantly inhibited proliferation of human pancreatic cancer cells (p<0.05). A substantial decrease in Akt phosphorylation was observed in carbon monoxide-releasing molecule compared with inactive carbon monoxide-releasing molecule treated cancer cells (by 30-50%, p<0.05). Simultaneously, carbon monoxide-releasing molecule and carbon monoxide exposure inhibited tumour proliferation and microvascular density of xenotransplanted tumours (p<0.01), and doubled the survival rates (p<0.005). Exposure of mice to carbon monoxide led to an almost 3-fold increase in carbon monoxide content in tumour tissues (p=0.006). CONCLUSION: These data suggest a new biological function for carbon monoxide in carcinogenesis, and point to the potential chemotherapeutic/chemoadjuvant use of carbon monoxide in pancreatic cancer.
Department of Biochemistry and Microbiology Institute of Chemical Technology Prague 6 Czech Republic
Queen's Medical Research Institute University of Edinburgh Edinburgh UK
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