Journal Article

PDGF AA as mediator in nicotine-dependent carcinogenesis

Eva M. Rakowicz-Szulczynska, David G. McIntosh, Michael Perry and McClure L. Smith

in Carcinogenesis

Volume 17, issue 9, pages 1813-1818
Published in print September 1996 | ISSN: 0143-3334
Published online September 1996 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.9.1813
PDGF AA as mediator in nicotine-dependent
                    carcinogenesis

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Effect of nicotine on PDGF AA and PDGF BB interaction with cervical cancer SiHa cells was tested. [125I]PDGF AA was internalized by cells and accumulated in the cytoplasm and nucleus (chromatin). In the absence of nicotine, maximal accumulation of [125I]PDGF AA inside the cells occurred after 1 day of incubation, which was followed by a progressive degradation of the growth factor during the next 2, 3 and 5 days of cell exposure. In the presence of 0.001 or 0.01% nicotine, accumulation of [125I]PDGF AA was slightly higher than in the absence of nicotine, and maximal accumulation occurred after 2 days of incubation. In the presence of 0.1% nicotine, maximal accumulation occurred after 5 days of incubation and was 20 and 14 times higher in the cytoplasm and chromatin, respectively. Nicotine-postponed degradation and increased nuclear accumulation of PDGF AA resulted in activation of RNA synthesis and cell proliferation. PDGF BB, which was not internalized by cells did not respond to nicotine treatment. The proposed mechanism of nicotine-PDGF AA co-carcinogenesis may involve inhibition of growth factor degradation at the lysosomal level and an increased chromatin accumulation of the non-degraded PDGF.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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