Acta NaturaeActa Naturae2075-8251Acta Naturae Ltd1058710.32607/20758251-2013-5-3-79-83Research ArticleCancer Specificity of Promoters of the Genes Involved in Cell Proliferation ControlKashkinK. N.kachkine@yandex.ruChernovI. P.kachkine@yandex.ruStukachevaE. A.kachkine@yandex.ruKopantzevE. P.kachkine@yandex.ruMonastyrskayaG. S.kachkine@yandex.ruUspenskayaN. Ya.kachkine@yandex.ruSverdlovE. D.kachkine@yandex.ruShemyakin-Ovchinnikov Institute of Bioorganic Chemistry1509201353798317012020Copyright © 2013, Kashkin K.N., Chernov I.P., Stukacheva E.A., Kopantzev E.P., Monastyrskaya G.S., Uspenskaya N.Y., Sverdlov E.D.2013<p>Core promoters with adjacent regions of the human genes CDC6, POLD1, CKS1B, MCM2, and PLK1 were cloned into a pGL3 vector in front of the Photinus pyrails gene Luc in order to study the tumor specificity of the promoters. The cloned promoters were compared in their ability to direct luciferase expression in different human cancer cells and in normal fibroblasts. The cancer-specific promoter BIRC5 and non-specific CMV immediately early gene promoter were used for comparison. All cloned promoters were shown to be substantially more active in cancer cells than in fibroblasts, while the PLK1 promoter was the most cancer-specific and promising one. The specificity of the promoters to cancer cells descended in the series PLK1, CKS1B, POLD1, MCM2, and CDC6. The bidirectional activity of the cloned CKS1B promoter was demonstrated. It apparently directs the expression of the SHC1 gene, which is located in a head-to-head position to the CKS1B gene in the human genome. This feature should be taken into account in future use of the CKS1B promoter. The cloned promoters may be used in artificial genetic constructions for cancer gene therapy.</p>promotercloningcancer-specificcancer gene therapyпромоторклонированиеопухолеспецифичностьгенная терапия опухолей[[1] Kawakami H., Katayama T. // Biochem Cell Biol. 2010, V.88, P.49-62][[2] Borlado L.R., Mendez J. // Carcinogenesis. 2008, V.29, P.237-243][[3] Lange S.S., Takata K., Wood R.D. // Nat Rev Cancer. 2011, №11, P.96-110][[4] Martinsson-Ahlzen H.S., Liberal V., Grunenfelder B., Chaves S.R., Spruck C.H., Reed S.I. // Mol Cell Biol. 2008, V.28, P.5698-5709][[5] Krishnan A., Nair S.A., Pillai M.R. // J Cell Mol Med. 2010, V.14, P.154-164][[6] Davila Lopez M., Martinez Guerra J.J., Samuelsson T. // PLoS One. 2010, V.5, P.e10654][[7] Rajendran M., Thomes P., Zhang L., Veeramani S., Lin M.F. // Cancer Metastasis Rev. 2010, V.29, P.207-222][[8] Masai H., You Z., Arai K. // IUBMB Life. 2005, V.57, P.323-335][[9] Song B., Liu X.S., Liu X. // Cell Div. 2012, V.7, P.3][[10] Zhang Y., Luoh S.M., Hon L.S., Baertsch R., Wood W.I., Zhang Z. // Nucleic Acids Res. 2007, V.35, P.152-158][[11] Kopantzev E.P., Vayshlya N.A., Kopantseva M.R., Egorov V.I., Pikunov M., Zinovyeva M.V., Vinogradova T.V., Zborovskaya I.B., Sverdlov E.D. // Br J Cancer. 2010, V.102, P.1533-1540][[12] Mityaev M.V., Kopantzev E.P., Buzdin A.A., Vinogradova T.V., Sverdlov E.D. // Biochemistry (Mosc). 2010, V.75, P.182-191]