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Tumor promoting properties of a cigarette smoke prevalent polycyclic aromatic hydrocarbon as indicated by the inhibition of gap junctional intercellular communication via phosphatidylcholine-specific phospholipase C
dc.creator | Upham, Brad L. | |
dc.creator | Blaha, Ludek | |
dc.creator | Babica, Pavel | |
dc.creator | Park, Joon-Suk | |
dc.creator | Sovadinova, Iva | |
dc.creator | Pudrith, Charles | |
dc.creator | Rummel, Alisa M. | |
dc.creator | Weis, Liliane M. | |
dc.creator | Sai, Kimie | |
dc.creator | Tithof, Patti K. | |
dc.creator | Gužvić, Miodrag | |
dc.creator | Vondracek, Jan | |
dc.creator | Machala, Miroslav | |
dc.creator | Trosko, James E. | |
dc.date.accessioned | 2018-03-01T20:21:17Z | |
dc.date.available | 2018-03-01T20:21:17Z | |
dc.date.issued | 2008 | |
dc.identifier.issn | 1347-9032 | |
dc.identifier.uri | https://vinar.vin.bg.ac.rs/handle/123456789/3396 | |
dc.description.abstract | Inhibition of gap junctional intercellular communication (GJIC) and the activation of intracellular mitogenic pathways are common hallmarks of epithelial derived cancer cells. We previously determined that the 1-methyl and not the 2-methyl isomer of anthracene, which are prominent cigarette smoke components, activated extracellular receptor kinase, and inhibited GJIC in WB-F344 rat liver epithelial cells. Using these same cells, we show that an immediate upstream response to 1-methylanthracene was a rapid ( LT 1 min) release of arachidonic acid. Inhibition of phosphatidylcholine-specific phospholipase C prevented the inhibition of GJIC by 1-methylanthracene. In contrast, inhibition of phosphatidylinositol specific phospholipase C, phospholipase A(2), diacylglycerol lipase, phospholipase D, protein kinase C, and tyrosine protein kinases had no effect on 1-methylanthracene-induced inhibition of GJIC. Inhibition of protein kinase A also prevented inhibition of GJIC by 1-methylanthracene. Direct measurement of phosphatidylcholine-specific phospholipase C and sphingomyelinase indicated that only phosphatidylcholine-specific phospholipase C was activated in response to 1-methylanthracene, while 2-methylanthracene had no effect. 1-methylanthracene also activated p38-mitogen activated protein kinase; however, like extracellular kinase, its activation was not involved in 1-methylanthracene-induced regulation of GJIC, and this activation was independent of phosphatidylcholine-specific phospholipase C. Although mitogen activated protein kinases were activated, Western blot analyzes indicated no change in connexin43 phosphorylation status. Our results indicate that phosphatidylcholine-specific phospholipase C is an important enzyme in the induction of a tumorigenic phenotype, namely the inhibition of GJIC; whereas mitogen activated protein kinases triggered in response to 1-methylanthracene, were not involved in the deregulation of GJIC. | en |
dc.relation | NIEHS NIH HHS [R01 ES013268, R01 ES013268-01A2], FIC NIH HHS [5D43 TW00641-10, D43 TW000641] | |
dc.rights | openAccess | en |
dc.source | Cancer Science | en |
dc.title | Tumor promoting properties of a cigarette smoke prevalent polycyclic aromatic hydrocarbon as indicated by the inhibition of gap junctional intercellular communication via phosphatidylcholine-specific phospholipase C | en |
dc.type | article | en |
dcterms.abstract | Упхам, Брад Л.; Парк, Јоон-Сук; Совадинова, Ива; Пудритх, Цхарлес; Руммел, Aлиса М.; Wеис, Лилиане М.; Саи, Кимие; Титхоф, Патти К.; Троско, Јамес Е.; Блаха, Лудек; Бабица, Павел; Гужвић Миодраг; Вондрацек, Јан; Мацхала, Мирослав; | |
dc.citation.volume | 99 | |
dc.citation.issue | 4 | |
dc.citation.spage | 696 | |
dc.citation.epage | 705 | |
dc.identifier.wos | 000254498800011 | |
dc.identifier.doi | 10.1111/j.1349-7006.2008.00752.x | |
dc.citation.rank | M22 | |
dc.identifier.pmid | 18377422 | |
dc.identifier.scopus | 2-s2.0-41249096480 | |
dc.identifier.fulltext | https://vinar.vin.bg.ac.rs//bitstream/id/4809/j.1349-7006.2008.00752.x.pdf |