"3247"^^ . "1"^^ . "Neuvedeno."@en . "0"^^ . "The molecular mechanism regulating anoikis (detachment-induced apoptosis) are not yet fully understood. The project follows up with our previous results showing interaction of polyunsaturated fatty acids (PUFAs) with butyrate and endogenous apoptotic inductors of TNF family with respect for cytokinetics of colon adenocarcinoma cell line HT-29. We suggest that lipid dietary components such as PUFAs cause permissive conditions for anoikis induction particularly by changes in cell membrane composition and oxidative metabolism. Crosstalks of individual signalling pathways induced by PUFAs, butyrate of TNF family molecules can lead to potentiation of apoptosis. Using cell lines in vitro derived from normal of cancer colon epihelia detailed mechanisms ofapoptosis after combined treatment of cells with agents mentioned above will be investigated. Special attention will be paid to the role of cell adhesion components and to crosstalk between mitochondria- and cell death receptor-mediated signalling"@en . "Mechanisms of the cell death induced by dietary lipid components and endogenous apoptotic regulators in colon epithelial cells"@en . . . . "Molekul\u00E1rn\u00ED mechanizmy reguluj\u00EDc\u00ED apopt\u00F3zu typu anoikis (indukovanou naru\u0161en\u00EDm kontaktu epiteli\u00E1ln\u00EDch bun\u011Bk st\u0159eva s extracelul\u00E1rn\u00ED matrix) jsou zat\u00EDm m\u00E1lo objasn\u011Bny. Projekt navazuje na na\u0161e p\u0159edchoz\u00ED v\u00FDsledky, kter\u00E9 odhalily interakce vysoce nenasycen\u00FDch mastn\u00FDch kyselin (VNMK) s butyr\u00E1tem a endogenn\u00EDmi induktory apopt\u00F3zy z rodiny TNF s ohledem na cytokinetiku linie adenokarcinomu kolonu HT-29. Vych\u00E1z\u00ED z p\u0159edpokladu, \u017Ee lipidov\u00E9 slo\u017Eky diety jako jsou VNMK mohou zejm\u00E9na zm\u011Bnami slo\u017Een\u00ED bun\u011B\u010Dn\u00FDch membr\u00E1n a oxidativn\u00EDho metabolizmu navodit podm\u00EDnky p\u0159\u00EDzniv\u00E9 pro indukci anoikis. Vz\u00E1jemn\u00E9 propojen\u00ED jednotliv\u00FDch sign\u00E1ln\u00EDch drah indukovan\u00FDch VNMK, butyr\u00E1tem nebo molekulami TNF rodiny m\u016F\u017Ee v\u00E9st k potenciaci apopt\u00F3zy. S vyu\u017Eit\u00EDm bun\u011B\u010Dn\u00FDch lini\u00ED odvozen\u00FDch z norm\u00E1ln\u00EDho i n\u00E1dorov\u00E9ho st\u0159evn\u00EDho epitelu budou in vitro studov\u00E1ny detailn\u00ED mechanizmy apopt\u00F3zy po kombinovan\u00E9m p\u016Fsoben\u00ED v\u00FD\u0161e jmenovan\u00FDch l\u00E1tek. D\u016Fraz bude kladen zejm\u00E9na na sledov\u00E1n\u00ED \u00FAlohy slo\u017Eek bun\u011B\u010Dn\u00E9 adheze a propojen\u00ED sign\u00E1ln\u00EDch"@cs . . "8"^^ . "Mechanizmy bun\u011B\u010Dn\u00E9 smrti st\u0159evn\u00EDch epiteli\u00E1ln\u00EDch bun\u011Bk indukovan\u00E9 lipidov\u00FDmi slo\u017Ekami v\u00FD\u017Eivy a endogenn\u00EDmi regul\u00E1tory apopt\u00F3zy"@cs . . . "8"^^ . . "3247"^^ . . "0"^^ . . . .