Potential for functional redundancy in EGF and TGFα signaling in desmoid cells: a cDNA microarray analysis

Abstract

Genes that replace or duplicate the function of other genes are considered functionally redundant. In this cDNA microarray study, using an Agilent microarray platform and GeneSifter™ analysis software, we evaluated (1) the degree of downstream transcriptional redundancy and (2) the level of genetic uniqueness apparent in desmoid tumor cells stimulated in vitro for 3 h or for 24 h with 100 ng/ml of exogenous recombinant human EGF (rhEGF) or with recombinant human transforming growth factor alpha (rhTGFα). Our intent was to identify genes costimulated, or genes unique to, desmoid cells stimulated in vitro with rhEGF and rhTGFα. This experimental approach demonstrated a 55% transcriptional redundancy in the number of desmoid genes significantly upregulated or downregulated following 3 h of stimulation with rhEGF or with rhTGFα, and a 65% transcriptional redundancy following 24 h of growth factor stimulation. Approximately 150 genes costimulated by rhEGF and rhTGFα were identified. This study suggests that EGF and TGFα retain some level of functional redundancy, possibly resulting from their divergence from a common ancestral gene.

Keywords::

• Epidermal growth factor
• transforming growth factor alpha
• functional redundancy
• cDNA microarray
• desmoid cells

Acknowledgements

This study was supported by research grants from the Desmoid Tumor Research Foundation (DTRF) and the Huntsman Cancer Foundation. The authors acknowledge the support provided by the Microarray Core Facility, Huntsman Cancer Institute, and the NCI Cancer Center support grant P30CA042014. We thank Kevin B. Jones for critical comments on this manuscript.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.