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• W1995185551 abstract "Background: Cancer cells can resist apoptosis that is induced by stimuli such as detachment or differentiation, but may be more susceptible to apoptosis when exposed to chemotherapeutic drugs. The pattern of gene expression that produces this phenotype is unknown. Methods: We compared gene expression patterns of normal human epidermal keratinocytes (NHEK cells) and the oral cancer cell line Tu183 when the cells were exposed to different apoptosis‐inducing stimuli. Results: Pathway analysis revealed that the phenotype difference could be best explained by the simultaneous existence of both proapoptosis and antiapoptosis signals in the cancer cells. Microarray analysis, supported by immunoblotting, showed that one gene that was likely to be involved in the proapoptosis signal was TNFRSF5 , which encodes the receptor CD40. When Tu183 cells were exposed to the CD40 ligand they showed apoptosis, while NHEK cells did not. Conclusions: The effects of different apoptotic stimuli on normal cells and oral cancer cells can be explained by expression of proapoptosis genes, including the gene that encodes CD40." @default.
• W1995185551 created "2016-06-24" @default.
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• W1995185551 date "2006-02-02" @default.
• W1995185551 modified "2023-10-15" @default.
• W1995185551 title "Analysis of apoptosis-associated genes and pathways in oral cancer cells" @default.
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• W1995185551 doi "https://doi.org/10.1111/j.1600-0714.2006.00398.x" @default.
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