Опухоль-промоторный эффект полициклических ароматических углеводородов (ПАУ)
Диссертация
Ингибирование МЩК в клетках гепатомы Г-27 под воздействием БП сочетается с падением уровня белка-супрессора р21, а в клетках гепатомы HepG2 с падением уровня белка-супрессора р27. Это свидетельствует о различных механизмах стимуляции клеточной пролиферации в указанных гепатомах. Провести сравнительное изучение действия канцерогенных ПАУ и их неканцерогенного аналога на функциональную активность… Читать ещё >
Содержание
- Введение 5 1. ОБЗОР ЛИТЕРАТУРЫ
- 1. 1. Механизмы химического канцерогенеза
- 1. 2. Химические канцерогены окружающей среды
- 1. 3. Механизмы активации непрямых канцерогенов
- 1. 4. Стимуляция пролиферации как необходимое звено опухолевой промоции. (
- 1. 5. Митогенный эффект активных форм кислорода
- 1. 6. Транскрипционный фактор NF-kB и его роль в пролиферации опухолевых клеток
- 1. 7. Межклеточные щелевые коммуникации и их ингибирование в ходе опухолевой промоции
- 1. 8. Апоптоз. 37 МАТЕРИАЛЫ И МЕТОДЫ ИССЛЕДОВАНИЯ
- 2. 1. Культура клеток
- 2. 2. Проницаемость щелевых контактов
- 2. 3. Определение уровня БП и БеП в клетках
- 2. 4. Реакция связывания NF-kB и АР-1 с консенсусным
- Олигонуклеотидом (Electrophoretic Mobility Shift Assay, EMSA)
- 2. 5. Электрофорез и Иммуноблотинг
- 2. 6. Транзиторная трансфекция и определение гена-репортера
- 2. 7. Определение влияния ПАУ на образование АФК в клетках гепатомы Г
- 3. РЕЗУЛЬТАТЫ
- 3. 1. Ингибирование межклеточных щелевых контактов при действии
- ПАУ в культуре клеток HepG
- 3. 2. Ингибирование межклеточных щелевых контактов
- ПАУ в культуре клеток Г
- 3. 3. Влияние ПАУ на экспрессию белков р21 и р
- 3. 4. Влияние ПАУ на активность NF-kB. а. Влияние ПАУ на транскрипционную активность NF-kB, определяемую методом транзиторной трансфекции. б. Влияние ПАУ на активацию NF-kB, определяемую методом EMS А
- 3. 5. Влияние ПАУ на активацию АР
- 3. 6. Влияние ПАУ на образование АФК. 72 4.0БСУЖДЕНИЕ
- 5. ВЫВОДЫ
Список литературы
- Белицкий Г. А. Будунова И.В. Культуры клеток печени мыши и человека как возможные объекты для ускоренного тестирования канцерогенных соединений // Экспериментальная онкология. — 1980. -№ 3. С. 39−46.
- Будунова И.В., Миттельман Л. А., Белицкий Г. А., Возможность выявления опухолевых промоторов по их ингибирующему действию на межклеточный обмен люциферовым желтым // Бюллетень экспериментальной онкологии и медицины. 1987. — № 11. — С. 717 719.
- Васильев Ю.М. Клетка как орхитектурное чудо. Ч. 2: Цитоскилет способный чувствовать и помнить // Соросовский образовательный журнал. — 1996. — № 4. — С. 4−10.
- Васильев Ю.М. Социальное поведение нормальных клеток и антисоциальное поведение опухолевых клеток. 2 Клетки строят ткань // Соросовский образовательный журнал. 1997. — № 5. — С. 20−25.
- Васильев Ю.М. Опухолевые клетки и их микроокружение.// Вопросы онкологии // 1984. № 30 920. — С. 96−103.
- Гельштейн В.И. Регуляция пролиферации нормальных и опухолевых клеток в культуре. Явления индукции и дифференцировки при опухолевом росте. М., 1981. — 340с.
- Гужаева E. J1. Роль индукторов цитохрома Р-450 в регуляции активности белков детоксикации ксенобиотиков и пролиферации клеток гепатом.// Дис К.м.н. 1998.
- Канцерогенез / под ред. Заридзе Д. Г. М.: Медицина, 2004.- 500 с.
- Кобляков В.А. Индукторы суперсемейства цитохрома Р-450, как промоторы канцерогенеза // Биохимия. 1998. — № 63. — С. 885−898.
- Кобляков В.А. Цитохром Р-450 в опухолях и в процессе канцерогенеза //Биохимия. 1995.-№ 60.-С. 1747−1764.
- Копнин Б.П. Онкгены, антионкогены и канцерогенез // Архив патологии. 1990. — № 9. — С. 3−12.
- Копнин Б.П. Мишени действия онкогенов и опухолевых супрессоров: ключ к пониманию базовых механизмов канцерогенеза // Биохимия. -2000. -№ 65. С. 5−33.
- Кулинский В.И. Обезвреживание ксенобиотиков // Соросовский образовательный журнал. 1999. — № 1. — С. 8−12.
- Пальцев М.А., Иванов А. А. Межклеточные взаимодействия М.: Медицина, 1998. — 288с.
- Пролемы экспериментальной онкологии лейкозов человека и животных / Под ред. JI.M. Шабада В. П. Шишкова. М.: Колос, — 1979. — 85с.
- Турусов B.C. Прогрессия опухолей: этиологические, морфологические и молекулярно-биологические аспекты // Архив патологии. -1992. № 7. -С. 5−14.
- Шапот B.C., Биохимические аспекты опухолевого роста. М: Медицина, 1975.-304с.
- Шапот B.C. Молекулярно-биологические аспекты неопластического превращения // Весстн. АМН СССР. 1979. — С. 48−55.
- Швемберг И.Н. Перевиваемый штамм гепатомы крысы Г-27 // Цитология. 1970. — № 12. — С. 1057−1059.
- Якубовская Р.И. Современные представления о механизмах канцкрогенеза и опухолевой прогрессии как основа для разработки новых методов терапии злокачественных новообразований // Российский онкологический журнал. 2000. — № 6. — С. 42−50.
- Abe J., Takahashi М., Ishida М., Lee J.D., Berc B.C. C-src is require for oxidative stress-mediated activation of big mitogen-activated protein kinase 1. // J. Biol. Chem., 1997, 15: 272, 20 389−20 394.
- Akintobi A.M., Villano C.M., White L.A. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure of normal human dermal fibroblasts results in
- AhR-dependent and -independent changes in gene expression. // Toxicol. Appl. Pharmacol. 2007, 1: 220, 9−17.
- Alberts В., Johnson A., Lewis J., Raff M., Roberts K., and Walter P. Molecular Biology of the Cell. 2002.
- L’Allemain G., Lavoie J.N., Rivard N., Baldin V., Pouyssegur J. Cyclin D1 expression is a major target of the cAMP-induced inhibition of cell cycle entry in fibroblasts. //Oncogene. 1997, 24:14, 1981−1990
- Baker Т.К., Kwiatkowski A.P., Madhukar B.V., Klaunig J.E. Inhibition of gap junctional intercellular communication by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rat hepatocytes. // Carcinogenesis, 1995, 16:23 212 326.
- Bauman J.W., Goldsworthy T.L., Dunn C.S., Fox T.R. Inhibitory effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on rat hepatocyte proliferation induced by 2/3 partial hepatectomy. // Cell Prolif., 1995, 28: 437−451.
- Bock K.W., Kohle C. Ah receptor- and TCDD-mediated liver tumor promotion: clonal selection and expansion of cells evading growth arrest and apoptosis. // Biochem. Pharmacol. 2005, 69:1403−1408.
- Beg A.A., Baltimore D. An essential role for NF-kappaB in preventing TNF-alpha-induced cell death. // Science, 1996, 1: 274, 782−784.
- Bennett M.V., Barrio L.C., Bargiello T.A., Spray D.C., Hertzberg E., Saez J.C. Gap Junctions: new tools, new answers, new questions. // Neuron 1991, 6:305−320.
- Berenblum I. Cancer research in historical perspective: an autobiographical essay. // Cancer Res. 1977, 37:1−7.
- Blaha L., Kapplova P., Vondracek J., Upham В., Machala M. Inhibition of gap-junctional intercellular communication by environmentally occurring polycyclic aromatic hydrocarbons. // Toxicol. Sci. 2002, 65:43−51.
- Blankenship A., Matsumura F. 2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced activation of a protein tyrosine kinase, pp60src, in murine hepatic cytosol using a cell-free system. // Mol. Pharmacol. 1997, 52:667−675.
- Boffetta P., Jourenkova N., Gustavsson P. Cancer risk from occupational and environmental exposure to polycyclic aromatic hydrocarbons. // Cancer Causes. Control., 1997, 8:444−472.
- Bohnenberger S., Wagner В., Schmitz H.J., Schrenk D. Inhibition of apoptosis in rat hepatocytes treated with 'non-dioxin-like' polychlorinated biphenyls. //Carcinogenesis. 2001, 22:1601−1606.
- Buchmann A., Stinchcombe S., Korner W., Hagenmaier H., Bock K.W. Effects of 2,3,7,8-tetrachloro- and 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin on the proliferation of preneoplastic liver cells in the rat. // Carcinogenesis, 1994, 15:1143−1150.
- Cascio M., Kumar N.M., Safarik R., Gilula N.B. Physical characterization of gap junction membrane connexons (hemi-channels) isolated from rat liver. //J. Biol. Chem., 1995, 270:18 643−18 648.
- Chapham D., and Schiller C. Dose-related effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in C57BL/6J and DBA/2J mice. // Toxicol. Appl. Pharmacol., 1985, 78:147−157.
- Chramostova K., Vondracek J., Sindlerova L., Vojtesek В., Kozubik A., Machala M. Polycyclic aromatic hydrocarbons modulate cell proliferation in rat hepatic epithelial stem-like WB-F344 cells. // Toxicol. Appl. Pharmacol., 2004, 196:136−148.
- Chen S.C., Pelletier D.B., Ao P., Boynton A.L. Boynton Connexin43 reverses the phenotype of transformed cells and alter their expression of cyclin/cyclin-depended kinases. // Cell Growth Differ., 1995, 6:681−690.
- Chen F., Castranova V., Shi X. New insights into the role of nuclear factor-kappaB in cell growth regulation. // Am. J. Pathol., 2001, 159:387−397.
- Christensen J.G., Gonzales A.J., Cattley R.C., Goldsworthy T.L. Regulation of apoptosis in mouse hepatocytes and alteration of apoptosis by nongenotoxic carcinogens. // Cell Growth Differ., 1998, 9:815−825.
- Conway J.G., Cattley R.C., Popp J.A., Butterworth B.E. Possible mechanisms in hepatocarcinogenesis by the peroxisome proliferator di (2-ethylhexyl)phthalate. // Drug. Metab. Rev., 1989, 21:65−102.
- Davis J., Lauer F., Burdick A., Hudson L., Burchiel S. Prevention of apoptosis by 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) in the MCF-10A cell line.//Cancer Res. 2001, 61:3314−3320.
- Dietrich C., Faust D., Budt S., Moskwa M., Kunz A., Bock K.W., Oesch F. 2,3,7,8-tetrachlorodibenzo-p-dioxin-dependent release from contact inhibition in WB-F344 cells: involvement of cyclin A. // Toxicol. Appl. Pharmacol. 2002, 183:117−26.
- Dogra S.C., Whitelaw M.L., May B.K. Transcriptional activation of cytochrome P450 genes by different classes of chemical inducers. // Clin. Exp. Pharmacol. Physiol., 1998, 25:1−9.
- Elferink C.J., Ge N.L., Levine A. Maximal aryl hydrocarbon receptor activity depends on an interaction with the retinoblastoma protein. // Mol. Pharmacol. 2001, 59:664−673.
- Ek-Vitorin, J. F., Calero G., Morley G. E., Coombs W., Taffet S.M., and Delmar M. PH regulation of connexin43: molecular analysis of the gating particle.//Biophys J. 1996, 71:1273−1284.
- Flohe L., Brigelius-Flohe R., Saliou C., Traber M.G., Packer L. Redox regulation of NF-kappa В activation. // Free Radic. Biol. Med., 1997, 22:1115−1126.
- Fitzegarld D.J., Mesnil M., Oyamada M., Tsuda H., Ito N. and Yamasaki H. Changes in gap junction protein (connexin32) gene expression during rat liver carcinogenesis. // J. Cell Biochem. 1989, 41:97−102.
- Gasparian A.V., Yao Y., Kowalezyk D., Lyakh L.A., Karseladze A., Slaga T And Budunova I.V. The role of IKK in constitutive activation of NF-kappaB transcription factor in prostate carcinoma cells. // J. Cell. Sci., 2002, 1:115, 141−151.
- Ge N., Elferink C. A direct interaction between the aryl hydrocarbon receptor and retinoblastoma protein. // J. Biol. Chem. 1998, 273:2 270 822 713.
- Gill J.H., James N.H., Roberts R.A., Dive C. The non-genotoxic hepatocarcinogen nafenopin suppresses rodent hepatocyte apoptosis induced by TGFbetal, DNA damage and Fas. // Carcinogenesis. 1998, 19:299−304.
- G6ttlicher M., Cikryt P., Wiebel F.J. Inhibition of growth by 2,3,7,8-tetrachlorodibenzo-p-dioxin in 5L rat hepatoma cells is associated with the presence of Ah receptor. // Carcinogenesis, 1990, 11:2205−2210.
- Hay den M.S., Ghosh S. Signaling to NF-kappaB. // Genes Dev., 2004, 15:18,2195−2224.
- Hess J., Angel P. and Schorpp-Kistner M. AP-1 subunits: quarrel and harmony among siblings. // Journal of Cell Science, 2004, 1 17:5965−5973.
- Hoffer A., Chang C.Y., Puga A. Dioxin induces transcription of fos and jun genes by Ah receptor-dependent and -independent pathways. // Toxicol. Appl Pharmacol., 1996, 141:238−47
- Holder, J.W., Elmore E. and Barrett J.C. Gap junction function and cancer. // Cancer Rec., 1993, 53:3475−3485.
- Huang G., Elferink C.J., Multiple mechanisms are involved in Ah receptor-mediated cell cycle arrest. // Mol. Pharmacol., 2005, 67:88−96.
- Jansen L.A., Jongen W.M. The use of initiated cells as a test system for the detection of inhibitors of gap junctional intercellular communication. // Carcinogenesis, 1996, 17:333−339.
- Janssen-Timmen U., Traub O., Dermitzel R., Rades H.M. and WiПеске К. Reduced number gap junction in hepatocarcinomas detected by monoclonal antibody. // Carcinogenesis, 1986, 7:1475−1482
- Jin D.Q., Jung J.W., Lee Y.S., Kim J.A. 2,3,7,8-Tetrachlorodibenzo-p-dioxin inhibits cell proliferation through arylhydrocarbon receptor-mediated G1 arrest in SK-N-SH human neuronal cells. // Neurosci. Lett., 2004,363:69−72.
- Kalimi G.H., Lo C.W. Communication compartments in the gastrulating mouse embryo. //J. Cell Biol., 1988, 107:241−255.
- Karin M., Cao Y., Greten F.R., Li Z.W. /NF-карраВ in cancer: from innocent bystander to major culprit. // Nat. Rev. Cancer, 2002, 2:301−310.
- Karin M. Nuclear factor-kappaB in cancer development and progression. // Nature, 2006, 25, 441:431−436.
- Karin M., Liu Z., Zandi E. AP-1 function and regulation. // Curr. Opin. Cell. Biol., 1997, 9:240−246.
- Kato J.Y., Matsuoka M., Polyak K., Massague J., Sherr C.J. Cyclic AMP-induced G1 phase arrest mrdiated by an inhibitor (pp7Kip 1) of cyclin-depenent kinase 4 activation. // Cell, 1994, 79:486−496.
- Kew M.C. Synergistic interaction between aflatoxin B1 and hepatitis В virus in hepatocarcinogenesis. // Liver Int., 2003, 23:405−409.
- Kim D.W., Gazourian L., Quadri S.A., Romieu-Mourez R., Sherr D.H., Sonenshein G.E. The RelA NF-карраВ subunit and the aryl hydrocarbonreceptor (AhR) cooperate to transactivate the c-myc promoter in mammary cells. // Oncogene, 2000, 16:19, 5498−5506.
- Kirk G.D., Bah E., Montesano R. Molecular epidemiology of human liver cancer: insights into etiology, pathogenesis and prevention from The Gambia, West Africa. // Carcinogenesis, 2006, 27:2070−2082.
- Kistler J., Bond J., Donaldson P., Engel A. Two distinct levels of gap junction assembly in vitro. // J. Struct. Biol., 1993, 110:28−38.
- Knerr S., Schaefer J., Both S., Mally A., Dekant W., Schrenk D. 2,3,7,8-Tetrachlorodibenzo-p-dioxin induced cytochrome P450s alter the formation of reactive oxygen species in liver cells. // Mol. Nutr. Food. Res., 2006, 50:378−384.
- K00 S.K., Kim D.Y., Park S.D., Kang K.W., Joe C.O., PKC phosphorilation disrupts gap junctional communication at GO/s phase in clone 9 cells. //Mol. Cell Biochem., 1997, 167:41−49.
- Kolluri S.K., Weiss C., Koff A., Gottlicher M. p27Kipl induction and inhibition of proliferation by the intracellular Ah receptor in developing thymus and hepatoma cells. // Genes Dev., 1999, 1:13, 1742−153.
- Krutovskikh V. and Yamasaki H. The role of gap junctional intercellular communications (GJIC) disorders in experimental and human carcinojenesis. // Histol. Histopatol., 1997, 12:761−768.
- Krutovskikh V.A. and Yamasaki H. /Ex vivo dye transfer assay as an approach to study gap junctional intercellular communication disorders in hepatorarcinogenesis. // Elsever Science, 1995: 93−97.
- Krutovskikh V.A., Oyamada M., Yamasaki H. Sequentional changes of gap junctions intercellular communications during multistage rat liver carcinogenesis: direct measurement of communication in vivo. // Carcinogenesis, 1991, 12:1701−1706.
- Laird D.W., Yancey S.B., Bugga L., Revel J.P. Connexin expression and gap junction communication compartments in the developing of mouse limb. //Dev. Dyn., 1992, 195:3725- 3734.
- Laird D.W. Connexin phosphorylation as a regulatory event linked to gap junction internalization and degradation. // Biochim. Biophys Acta., 2005, 10: 1711, 172−182.
- Lake B.G. Mechanisms of hepatocarcinogenicity of peroxisome-proliferating drugs and chemicals. // Annu. Rev. Pharmacol. Toxicol., 1995, 35:483−507.
- Lampe P.D., Lau A.F. Regulation of gap junctions by phosphorylation of connexins. // Arch. Biochem. Biophys., 2000, 15:384, 205−215.
- Lawrence T.S., Beers W.H., Gilula N.B. Transmission of hormonal stimulation by cell-cell communication. //Nature, 1978, 272:501−506.
- Lee S.F., Huang Y.T., Wu W.S., Lin J.K. Induction of c-jun protooncogene expression by hydrogen peroxide through hydroxyl radical generation and p60SRC tyrosine kinase activation. II Free Radic. Biol. Med., 1996, 21:437 448.
- Lee S.W., Tomasetto C., Paul D., Keyomarsi K. and Sager R. Transcriptional downregulation of gap junction proteins blocks junctional communications in human mammary tumor cell lines. I/ J. Cell Biol., 1992, 188:1213−1221.
- Loewenstein W.R. Junctional intercellular communication: the cell-cell membrane channel. //Physiol. Rev., 1981, 61:829−913.
- Li Y., Leung L.K., Spear B. T, Glauter H.P. Activation of hepatic NF-kappaB by phenobarbital in rats. // Biochem. Biophys. Res. Commun., 1996, 229:982−989.
- Li J., Chen H., Ke Q., Feng Z., Tang MS., Liu В., Amin S., Costa M., Huang C. Differential effects of polycyclic aromatic hydrocarbons on transactivation of AP-1 and NF-kappaB in mouse epidermal cl41 cells. // Mol. Carcinog., 2004, 40:104−115.
- Ma C., Wang J., Luo J. Activation of nuclear factor kappa В by diesel exhaust particles in mouse epidermal cells through phosphatidylinositol 3kinase/Akt signaling pathway. I I Biochem, Pharmacol., 2004, 15:67, 19 751 983.
- Melendez-Colon V.J., Luch A., Seidel A., Baird W.M. Cancer initiation by polycyclic aromatic hydrocarbons results from formation of stable DNA adducts rather than apurinic sites. // Carcinogenesis, 1999, 20:1885−1891.
- Mehta P.P., Hotz-Wagenblatt A., Rose В., Shalloway D., Loewenstein W.R. Incorporation of the gene for cell-cell channel protein into transformed cells leads to nonnalization of the growth. // J. Membr. Biol., 1991, 124:207−225.
- Mehta P.P., Bertram J.S., Loewenstein W.R. Growth inhibition of transformed cells correlates with their junctional communication with normal cells. // Cell, 1986, 44:187−96.
- Mesnil M., Krutovskikh V., Piccoli C., Elfgang C., Traub O., Willecke K., Yamasaki H. Negative growth control of HeLa cells by connexin genes: connexin species specifity. // Cancer Res., 1995, 1: 55, 629−639.
- Nebert D.W., Puga A., Vasiliou V. Role of the Ah receptor and the dioxin-inducible Ah. gene battery in toxicity, cancer, and signal transduction. //Ann. N. Y. Acad. Sci., 1993, 23:685, 624−640.
- Murray S.A., Fletcher W.H. Hormone-induced intercellular signal transfer dissociates cyclic amp-dependent protein kinase. // J. Cell. Biol., 1984, 98:1710−1719.
- Neumann H.G. Aromatic amines in experimental cancer research: tissue-specific effects, an old problem and new solutions. // Crit. Rev. Toxicol., 2007,37:211−236.
- Neumann H.G., Hammerl R., Hillesheim W., Wildschutte M. Role of genotoxic and nongenotoxic effects in multistage carcinogenicity of aromatic amines. // Environ. Health Perspect., 1990, 88:207−211.
- Neveu M., Hully J., Paul D. and Pitot H. Reversible alterations in the expression of the gap junctional protein connexine32 during tumor promotion in rat liver and its role during cell proliferanion. // Cancer Communic., 1990, 2:21−31.
- Neveu M.J., Babcock K.L., Hertzberg E.L., Paul D.L., Nicholson B.J., Pitot H.C. Colocalized alterations in connexin32 and cytochrome P450IIB½ by phenobarbital and related liver tumor promoters. // Cancer Res., 1994, 15:54,3145−3152.
- Neveu M.J., Hully J.R., Babcock K.L., Hertzberg E.L., Nicholson В .J., Paul D.L., Pitot H.C. Multiple mechanisms are responsible for altered expression of gap junction genes during oncogenesis in rat liver. // J. Cell Sci., 1994, 107:83−95.
- Nicholson В., Dermietzel R., Teplow D., Traub O., Willecke K., Revel J.P. Two homologous protein components of hepatic gap junction. // Nature, 1987, 329:732−734.
- Ohde G., Schuppler J., Schulte-Hermann R., Keiger H. Proliferation of rat liver cells in preneoplastic nodules after stimulation of liver growth by xenobiotic inducers. //Arch. Toxicol. Suppl., 1979, 2:451−455.
- Omori Y., Krutovskikh V., Mironov N., Tsuda H., Yamasaki H. Cx32 gene mutation in chemically-induced rat liver tumor. // Carcinogenesis, 1996, 17:2077−2080.
- Omori Y., Mesnil M., Yamasaki H. Connexin32 mutations from X-linked Charot- Marie-Tooth disease patients- functional defects and dominant-negative effects. // Mol. Biol. Cell, 1996, 7:907−916.
- Park J.Y., Shigenaga M.K., Ames B.N. Induction of cytochrome P4501A1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin or indolo (3,2-b)carbazole is associated with oxidative DNA damage. // Proc. Natl. Acad. Sci. USA, 1996, 19:93,2322−2327.
- Pastan I.H., Johnson G.S., Anderson W.B. Role of cyclic nucleotides in growth control. // Annu Rev Biochem., 1975, 44:491−522.
- Pei X.H., Nakanishi Y., Inoue H., Takayama K., Bai F., Hara N. Polycyclic aromatic hydrocarbons induce IL-8 expression through nuclear factor kappaB activation in A549 cell line. // Cytokine, 2002, 19:236−41.
- Pei X.H., Nakanishi Y., Takayama K., Bai F., Hara N. Benzoa. pyrene activates the human p53 gene through induction of nuclear factor kappaB activity. // J. Biol. Chem., 1999, 3:274, 35 240−35 246.
- Puga A., Barnes S.J., Chang C., Zhu H., Nephew K.P., Khan S.A., Shertzer H.G. Activation of transcription factors activator protein-1 and nuclear factor-kappaB by 2,3,7,8-tetrachlorodibenzo-p-dioxin. // Biochem. Pharmacol., 2000, 58:997−1005.
- Ren P., Mehta P.P., Ruch R.J. Inhibition of gap junctional intercellular communication by tumor promoters in connexin43 andconnexin32-expressing liver cells: cell specificity and role of protein kinase C.//Carcinogenesis. 1998, 19:169−175.
- Ren P., Ruch R.J. Inhibition of gap junction intercellular communication by barbiturates in long- term primary cultured rat hepatocytes is correlated with liver tumor promoting activity. // Carcinogenesis, 1996, 17:2119−2124.
- Risek В., Klier F.G. and Gilula N.B. Developmental regulation and structural organization of connexins in epidermal gap junctions. // Dev. Biol., 1994, 164:183−196.
- Saez J.C., Martinex A.D., Branez M.C., Conzalez H.E. Regulation of gap junction by protein phosphorilation. // Braz. J. Med. Biol. Res., 1998, 31:593−600.
- Sakamoto H., Oyamada M., Enomoto K. and Mori M. Differential changes in expression of gap junctions protein connexin26 and 32 during hepatocarcinojenesis in rats. //Jpn. J. Cancer Res., 1992, 83:1210−1215.
- Sanson M., Marcaud V., Robin E., Valery C., Sturtz F., Zalc B. Connexin 43-mediated bystander effect in two rat glioma cell. // Cancer Gene Ther., 2002, 9:149−155.
- Savas U., Griffin K.J., Johnson E.F. Molecular mechanisms of cytochrome P-450 induction by xenobiotics: An expanded role for nuclear hormone receptors. // Mol. Pharmacol., 1999, 56:851−857.
- Schmidt K.N., Amstad P., Cerutti P., Baeurle P.A. The roles of hydrogen peroxide and superoxide as messengers in the activation of transcription factor NF-kappa B. // Chem. Biol., 1995, 2:13−22.
- Schrenc D., Schmitz H.J., Bohnenberger S., Wagner В., Womer W. Tumor promoters as inhibitors of apoptosis in rat hepatocytes. // Toxicol. Lett., 2004, 149:43−50.
- Schrenk D., Karger A., Lipp H.P., Bock K.W. 2,3,7,8-Tetrachlorodibenzo-p-dioxin and ethinylestradiol as co-mitogens in cultured rat hepatocytes.// Carcinogenesis, 1992, 13:453−456.
- Schuller H.M., Orloff M. Tobacco-specific carcinogenic nitrosamines. Ligands for nicotinic acetylcholine receptors in human lung cancer cells. //Biochem. Pharmacol., 1998, 55:1377−1384.
- Schuller H.M. Nitrosamines as nicotinic receptor ligands. // Life Sci., 2007, 30:80, 2274−2280.
- Schwarz M., Buchmann A., Bock K.W. Role of cell proliferation at early stages of hepatocarcinogenesis. // Toxicol. Lett., 1995, 82−83:27−32.
- Shaulian E., Karin M. AP-1 in cell proliferation and survival. //
- Oncogene, 2001, 30:20, 2390−2400.
- Shipley J.M., Waxman D.J. Aryl hydrocarbon receptor-independent activation of estrogen receptor-dependent transcription by 3-methylcholantrene. // Toxicol. Appl. Pharmacol., 2006, 213:87−97.
- Shubik, P. The growth potentialities of induced skin tumors in mice. The effects of different methods of chemical carcinogenesis. // Cancer Res., 1950 10:713−717.
- Solan J.L., Lampe P.D. Connexin phosphorylation as a regulatory event linked to gap junction channel assembly. // Biochim. Biophys. Acta., 2005, 10:1711, 154−163.
- Solhaug A., Refsnes M., Lag M., Schwarze P., Husoy Т., Holme J. Polycyclic aromatic hydrocarbons induce both apoptotic and anti-apoptotic signals in Hepalclc7 cells. // Carcinogenesis, 2004, 25:809−819.
- Spray D.C., Moreno A.P., Kessler J.A. and Dermietzel R. Characterization of gap junction between cultured leptominengeal cells. // Brain Res., 1991, 568:1−14.
- Stauffer K.A. The gap junction proteins Bl-connecsin (connecsin-32) and B2-connecsin (connecsin-26) can form heteromeric hemichannels. // J. Biol. Chem., 1995, 270:6768−6772.
- Stauffer K.A., Kumar N.M., Gilula N.B., Unwin N. /Isolation and purification of gap junction channels.//J. Cell Biol., 1991, 115: 141−150.
- Tan Z., Chang X., Puga A., Xia Y. Activation of mitogen-activated protein kinases (MAPKs) by aromatic hydrocarbons: role in the regulation of aryl hydrocarbon receptor (AHR) function. // Biochem. Pharmacol., 2002, 64:771−780.
- Tanaka Т., Yamasaki H., Mesnil M., Induction of bystander effect in HeLa cells by using a bigenic vector carrying viral thymidine kynase and connexin32 genes. // Mol. Carcinogen., 2001, 30:176−180.
- Tannheimer S.L., Barton S.L., Ethier S.P., Burchiel S.W. Carcinogenic polycyclic aromatic hydrocarbons increase intracellular Ca2+ and cell proliferation in primary human mammary epithelial cells. // Carcinogenesis, 1997, 18:1177−1 182.
- Tateno С., Ito S., Tanaka M., Oyamada M. and Yoshitake A. Effect of TCDD on hepatic gap junction intercellular communication in rats. // Carcinogenesis, 1994, 15:517−521.
- Tharappel J.C., Cunningham M.L., Spear B.T., Glauert H.P. Differential activation of hepatic NF-kappaB in rats and hamsters by the peroxisome proliferators Wy-14,643, gemfibrozil, and dibutyl phthalate. // Toxicol. Sci., 2001, 62:20−27.
- Thilly W. Have environmental mutagens caused oncomutations in people? //Nature Genetics, 2003, 34:253−258.
- Tian Y., Ke S., Denison M.S. Rabson A. B. and Gallo M. A. Ah Receptor and NF-B Interactions, a Potential Mechanism for Dioxin Toxicity. //J. Biol. Chem., 1999, 274: 1,510−515.
- Tian Y., Rabson A.B., Gallo M.A. Ah receptor and NF-kappaB interactions: mechanisms and physiological implications. // Chem. Biol. Interact., 2002, 20:141, 97−115.
- Traub O., Look J., Dermietzel R., Brummer F., Hulser D. and Willecke K. Comparative characterization of the 21 kD and 26 kD gap junction proteins in murine liver and cultured hepatosytes. // J. Cell Biol., 1989, 108:1039−1051.
- Trosko J.E. and Goodman J.I. Intercellular communication may facilitate apoptosis: implications of tumor promotion. // Mol. Cancinogen., 1994, 11:8−12.
- Trosko J.E., Ruch R.J. Cell-cell communication in carcinogenesis. // Front Biosci., 1998, 15:208−236.
- Turpaev K.T. Role of transcription factor AP-1 in integration of cellular signalling systems. // Mol. Biol. (Mosk). 2006, 40:945−961.
- Upham В., KoskiT., Rummel A., Wilson M., Horvath A., Trosko J.E. Differential roles of 2, 6, and 8 carbon ceramides on the modulation of gap junctional communication and apoptosis during carcinogenesis. // Cancel-Lett., 2003, 191:27−34.
- Upham B.L., Weis L.M., Rummel A.M., Masten S.J., Trosko J.E. The effects of anthracene and methylated anthracenes on gap junctional intercellular communication in rat liver epithelial cells. // Fundam. Appl. Toxicol., 1996, 34:260−264.
- Vaziri C., Faller D.V. A benzoa. pyrene-induced cell cycle checkpoint resulting in p53-independent G1 arrest in 3T3 fibroblasts. // J. Biol. Chem., 1997, 272:2762−2791.
- Vrzal R., Ulrichova J., Dvorak Z. Aromatic hydrocarbon receptor status in the metabolism of xenobiotics under normal and pathophysiological conditions. // Biomed. Pap. Med. Fac. Univ. Palacky., 2004, 148:3−10.
- Wilson C.L., Safe S. Mechanisms of ligand-induced aryl hydrocarbon receptor-mediated biochemical and toxic responses. // Toxicol. Pathol., 1998, 26:657−671.
- Witlock J. Genetic and molecular aspects of 2,3,7,8-tetrachlorodibenzo-p-dioxin action. Ann. Rev. // Pharm. Toxicol., 1990, 30:251−277.
- Whitlock J.P. Jr., Okino S.T., Dong L., Ко H.P., Clarke-Katzenberg R., Ma Q., Li H. Cytochromes P450 5: induction of cytochrome P4501A1: a model for analyzing mammalian gene transcription. // FASEB J., 1996 10:809−818.
- Whitfield J.F., Boynton A.L., MacManus J.P., Sikorska M., Tsang B.K. The regulation of cell proliferation by calcium and cyclic AMP. // Mol. Cell Biochem., 1979, 27:155−179.
- Worner W., Schrenc D. Influence of liver tumor promoters on apoptosis in rat hepatocytes induced by 2-acetylaminofluorene, ultraviolet light, or transforming growth factor beta 1. // Cancer Res., 1996, 56, p.1272−1278.
- Weis L.M., Rummel A.M., Masten S.J., Trosko J.E., Upham B.L. Bay or baylike regions of polycyclic aromatic hydrocarbons were potent inhibitors of Gap junctional intercellular communication. // Environ. Health Perspect., 1998, 106:17−22.
- Wolfle D., Becker E., Schmutte C. Growth stimulation of primary rat hepatocytes by 2,3,7,8-tetrachlorodibenzo-p-dioxin. // Cell Biol. Toxicol., 1993, 9:15−31.