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Signal transduction of EGF‐enhenced Aurora‐A expression in A431 cells
Author(s) -
Hung LiangYi,
Wu MinLi,
Chang WenChang
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a468
Subject(s) - signal transduction , a431 cells , microbiology and biotechnology , transduction (biophysics) , expression (computer science) , biology , cell , computer science , genetics , biophysics , cell cycle , oncogene , programming language
Human Aurora‐A kinase and epidermal growth factor receptor (EGFR) both are highly expressed in a lot of malignant tumors and cancer cell lines. According the documents previously reported, the human Aurora‐A gene is a potential oncogene. The increased level of human Aurora‐A kinase in malignant tumors and cancer cell lines is through the DNA amplification, protein stabilization and transcriptional up‐regulation. But the detailed mechanism of transcriptional regulation of human Aurora‐A gene in tumors is still unclear. In recently years, the nuclear localization of epidermal growth factor receptor (EGFR) has been demonstrated by many groups. The nuclear location of EGFR is strongly correlated with highly proliferating activity and where it functions as a transcription activator. The human epidermoid carcinoma cell line A431 expressed a high level of EGFR and some of the EGFR are nuclear located. In our preliminary results, when treated four cultured cell lines (293T, A431, HeLa and MCF7) with EGF, only in A431 cells, which expressed high level of EGFR, the Aurora‐A kinase is up‐regulated. In addition, the ChIP assay also demonstrated that EGFR can bind to the promoter region of Aurora‐A gene. The relationship between the transcriptional regulation of Aurora‐A gene and EGFR in tumors is currently investigated.