Analysis of the role of p38 MAP kinase in epidermal growth factor-induced JB6 Cl41 cell transformation by cDNA array

To further explore the mechanism of p38 MAP kinase in regulation of JB6 Cl41 cell transformation. cDNA array was employed to scan the differential expression genes between DN-p38 cells and CMV-neo JB6 Cl41 cells after EGF stimuli. We found that up-expression genes including oncogenes and tumor suppressor genes, p53-associated protein, transcription repressors, apoptosis-associated genes, and growth arrest and DNA damage-inducible protein 153 were detected in DN-p38 cells, but low expression in CMV-neo JB6 Cl41 cells after EGF treatment. Meanwhile, some proto-oncogenes, such as c-Myc, and signal transducer and activator of transcription 1 (STAT1) were lowly expressed in EGF-stimulated DN-p38 cells, but had relatively high expression level in CMV-neo JB6 Cl41 cells under the same stimuli. Four of the differential expression genes were further confirmed by quantitative RT-PCR analysis. Our results indicate that p38 MAP kinase is involved in EGF-induced JB6 Cl41 cell transformation through effecting on more genes expression levels including transcription factors, proto-oncogene, apoptosis-related genes and growth arrest genes.

► We found that more genes and pathways are regulated by p38 MAP kinase.
► p38 MAP kinase plays a key role in the EGF-induced JB6 Cl41 cell transformation.
► p38 MAP kinase may be a target in cancer prevention.
► cDNA array is still a useful tool for finding new targets at transcription level.