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Effects of Nicotinamide on Mouse Skin Tumor Development and Its Mode of Action

Biomedical and Environmental Sciences 1999年第3期12卷 177-187页

作者： KRISHNA P. GUPTA(Environmental Carcinogenesis Section, Industrial Toxicology Research Centre,Post Box No- 80, Mahatma Gandhi Mang, Lucknow-226 001, India) Environmental Carcinogenesis Section Indust. Toxicology Research Centre Mahatma Gandhi Marg Lucknow-226 001 India

Nicotinamide (NA), a naturally occuring vitamin and a protease inhibitor, has been shown to be effective in treating some skin ailments. It inhibits cell proiferaion and induces cell differentiation. This report shows the effects of NA on mouse skin tumor development and on the critical events involved in this process. NA reduced tumor growth, inhibited the 12-O-tetradecanoylphorbol-13-acetate (TPA) induced ornithine decarboxylase activity, but induced the transglutaminare activity which was inhibited by TPA under different experimental *** effects of NA on ornithine decarboxylare (ODC) and transglutaminase (TG) indicated that nicotinamide (NA) probably programmmed the cells for their death in the natural course of time, i.e. programed cell death. This observation indicates that NA might be a better agent for the detailed study and for the better use in prevention of cancer alone or in combination with other drugs.

关键词： Apoptosis Animals Female Mice Niacinamide Ornithine Decarboxylase Research Support, Non-U.S. Gov't Skin Neoplasms tetradecanoylphorbol acetate Transglutaminases

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Epstein-Barr virus induces human nasopharyngeal epithelial cells to escape from the replicative senescence

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Chinese Medical Journal 2002年第6期115卷 803-809,146页

作者：杨静唐发清顾焕华邓锡云翁新宪唐敏曹亚湖南医科大学肿瘤研究所长沙410078

OBJECTIVE: To observe the biological changes of primary human nasopharyngeal epithelial cells in the early stage of immortalization. METHODS: The morphological changes of nasopharyngeal epithelial cells were observed by phase contrast microscopy, and the activity profile of senescence-associated beta-galactosidase (SA-beta-Gal) was detected by SA-beta-Gal staining. The expression of p16(INK4a) protein was tested by immunochemical assay, and the life span in vitro of nasopharyngeal epithelial cells was calculated as population doublings. In addition, the expression of Epstein-Barr (EB) virus latent membrane protein 1 (LMP1) was also detected by immunofluorescence staining. RESULTS: Morphologically, cells treated with EB virus and 12-o-tetradecanoyl-phorbol-13-acetate (TPA) formed multi-layer foci, and their cellular life span in vitro was extended (about 155 days of culture). A low percentage of cells (about 4.8%) expressed SA-beta-Gal activity at late primary culture, and did not always express p16(INK4a) protein in the progression of culture. CONCLUSIONS: Nasopharyngeal epithelial cells treated with EB virus in cooperation with TPA can pass through the stage of senescence and enter the early stage of immortalization. Some changes of phenotype occur in these *** results provide data for further studying the mechanism of immortalization and the establishment of a human nasopharyngeal epithelial cell line.

关键词： Cell Aging Cell Transformation, Viral Cyclin-Dependent Kinase Inhibitor p16 Epithelial Cells Herpesvirus 4, Human Humans Nasopharynx Research Support, Non-U.S. Gov't tetradecanoylphorbol acetate

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Induction of apoptosis by TPA and VP-16 is through translocation of TR3

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World Journal of Gastroenterology 2002年第3期8卷 446-450页

作者： LiuS WuQ 等 KeyLaboratoryoftheMinistryofEducationforCellBiologyandTumorCellEngineering SchoolofLifeSciencesXiamenUniversityXiamen361005FujianProvinceChina KeyLaboratoryoftheMinistryofEducationforCellBiologyan

AIM: To investigate the role of TR3 in induction of apoptosis in gastric cancer cells. METHODS: Human gastric cancer cell line, MGC80-3, was used. Expression of TR3 mRNA and its protein was detected by Northern blot and Western blot. Localization of TR3 protein was showed by immunofluorescence analysis under laser-scanning confocal microscope. Apoptotic morphology was observed by DAPI fluorescence staining, and apoptotic index was counted among 1000 cells randomly. Stable transfection assay was carried out by Lipofectamine. RESULTS: Treatment of MGC80-3 cells with TPA and VP-16 resulted in apoptosis, accompanied by the repression of Bcl-2 protein in a time-dependent manner. At the same time, TPA and VP-16 also up-regulated expression level of TR3 mRNA in MGC80-3 cells that expressed TR3 mRNA. When antisense-TR3 expression vector was transfected into the cells, expression of TR3 protein was repressed. In this case, TPA and VP-16 did not induce apoptosis. In addition, TPA and VP-16-induced apoptosis involved in translocation of TR3. In MGC80-3 cells, TR3 localized concentrative in nucleus, after treatment of cells with TPA and VP-16, TR3 translocated from nucleus to cytosol obviously. However, when this nuclear translocation was blocked by LMB, apoptosis was not occurred in MGC80-3 cells even in the presence of TPA and VP-16. CONCLUSION: Induction of apoptosis by TPA and VP-16 is through induction of TR3 expression and translocation of TR3 from nucleus to cytosol, which may be a novel signal pathway for TR3, and represent the new biological function of TR3 to exert its effect on apoptosis in gastric cancer cells.

关键词： Active Transport, Cell Nucleus Apoptosis DNA-Binding Proteins Etoposide Gene Expression RNA, Messenger RNA, Neoplasm Receptors, Cytoplasmic and Nuclear Receptors, Steroid Research Support, Non-U.S. Gov't Signal Transduction Stomach Neoplasms tetradecanoylphorbol acetate Transcription Factors Tumor Cells, Cultured

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