“3-O-Methylfunicone, a secondary metabolite produced by Penicillium piniphilum, induces growth arrest and apoptosis in HeLa cells” (Articolo in rivista)

Type
Label
  • “3-O-Methylfunicone, a secondary metabolite produced by Penicillium piniphilum, induces growth arrest and apoptosis in HeLa cells” (Articolo in rivista) (literal)
Anno
  • 2004-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1111/j.1365-2184.2004.00323.x (literal)
Alternative label
  • E. Buommino, R. Nicoletti, G. M. Gaeta, M. Orlando, M. L. Ciavatta, A. Baroni and M. A. Tufano (2004)
    “3-O-Methylfunicone, a secondary metabolite produced by Penicillium piniphilum, induces growth arrest and apoptosis in HeLa cells”
    in Cell proliferation (Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • E. Buommino, R. Nicoletti, G. M. Gaeta, M. Orlando, M. L. Ciavatta, A. Baroni and M. A. Tufano (literal)
Pagina inizio
  • 413 (literal)
Pagina fine
  • 426 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 37 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Department of Experimental Medicine, Section of Microbiology and Clinical Microbiology, Second University of Naples, Tobacco Experiment Institute, Scafati, Department of Odontostomatological, Ortodontical and Surgical Disciplines, Second University of Naples, Institute of Biomolecular Chemistry, CNR, Pozzuoli and Department of Dermatology, Second University of Naples, Italy (literal)
Titolo
  • “3-O-Methylfunicone, a secondary metabolite produced by Penicillium piniphilum, induces growth arrest and apoptosis in HeLa cells” (literal)
Abstract
  • 3- O -Methylfunicone (OMF) is a secondary metabolite produced by the soil fungus Penicillium pinophilum which has cytostatic properties. The aim of this study was to investigate the mechanisms by which such properties are exerted, with special reference to any anti-proliferative and apoptotic potential, on HeLa cells. OMF treatment caused about 44% inhibition of cell growth after 24 h, and modifications in the tubulin fibre organization. In addition, a significant increase in p21 mRNA expression and a decrease in cyclin D1 and Cdk4 mRNA expression resulted at the same time. Apoptosis induction was demonstrated by the annexin V assay, cytofluorimetric analysis of the DNA content of the sub-G 1 fraction and DNA laddering. Taken together, our data showed that the compound inhibits proliferation of HeLa cells by several mechanisms, such as disruption of tubulin fibres, cell cycle arrest and apoptosis induction. The capacity of the compound to affect the cell cycle and to modulate apoptosis is indicative of a potential for the development of a new agent for cancer chemotherapy. (literal)
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Autore CNR

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