PURPOSE: The aim of the present study was to identify genes regulated in the early response to heat-shock in human head-and-neck cancer cells using a cDNA array. METHODS AND MATERIALS: IMC-3 cells were heat-shocked at 44 degrees C for 30 min, then incubated for 6 h. After 6 h incubation, mRNAs were extracted. Early gene expressions in IMC-3 cells were analyzed using a cDNA array after heat-shock. In addition, reverse transcription-polymerase chain reaction (RT-PCR) was performed to identify the expressions of mRNA for confirming features by cDNA array analysis in several other cell lines (KB, T3M-1, SCC-TF) as well as in IMC-3 cells. RESULTS: Twenty-eight genes were found to be induced or upregulated by heat-shock in IMC-3 cells. These included genes involved in the apoptosis (e.g., CC3, caspase10), tumor invasion (e.g., CC3, TIMP-3), cell cycle checkpoint control (e.g., DP-1, CDC25A), signal transduction (e.g., MEK1) as well as genes associated with heat stress (e.g., Hsp70B', Hsp40). Gene expressions of CC3 and MEK1 were recognized to be induced by heat-shock in pharyngeal cancer cells (KB, T3M-1) and lingual cancer cells (SCC-TF). CONCLUSION: The observed alteration in gene expression may play a role in various biochemical pathways of cancer cells exposed to heat-shock.
PURPOSE: The aim of the present study was to identify genes regulated in the early response to heat-shock in human head-and-neck cancer cells using a cDNA array. METHODS AND MATERIALS: IMC-3 cells were heat-shocked at 44 degrees C for 30 min, then incubated for 6 h. After 6 h incubation, mRNAs were extracted. Early gene expressions in IMC-3 cells were analyzed using a cDNA array after heat-shock. In addition, reverse transcription-polymerase chain reaction (RT-PCR) was performed to identify the expressions of mRNA for confirming features by cDNA array analysis in several other cell lines (KB, T3M-1, SCC-TF) as well as in IMC-3 cells. RESULTS: Twenty-eight genes were found to be induced or upregulated by heat-shock in IMC-3 cells. These included genes involved in the apoptosis (e.g., CC3, caspase10), tumor invasion (e.g., CC3, TIMP-3), cell cycle checkpoint control (e.g., DP-1, CDC25A), signal transduction (e.g., MEK1) as well as genes associated with heat stress (e.g., Hsp70B', Hsp40). Gene expressions of CC3 and MEK1 were recognized to be induced by heat-shock in pharyngeal cancer cells (KB, T3M-1) and lingual cancer cells (SCC-TF). CONCLUSION: The observed alteration in gene expression may play a role in various biochemical pathways of cancer cells exposed to heat-shock.