http://www.cnr.it/ontology/cnr/individuo/prodotto/ID14992
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
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- 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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