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Multimodality expression profiling shows SEPT9 to be overexpressed in a wide range of human tumours

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Abstract

Septins are an evolutionarily conserved family of GTPases with diverse functions including roles in cytokinesis that have been implicated in neoplasia. To address the potential role of SEPT9 in tumorigenesis, we assessed the expression of SEPT9 in 7287 fresh frozen human tissue samples and 292 human cell lines by microarray analysis. In addition, we used a sensitive RT–PCR strategy to define the expression of SEPT9 isoforms in archival formalin-fixed and paraffin-embedded normal human tissues. The mRNA data were further confirmed by immunohistological analyses of SEPT9 protein expression in normal human tissues using antisera that detect SEPT9 isoforms. Using these complementary approaches, we demonstrate that SEPT9 mRNA and protein are expressed ubiquitously, with the isoforms showing tissue-specific expression. The microarray analysis indicates that there is consistent overexpression of SEPT9 in diverse human tumours including breast, CNS, endometrium, kidney, liver, lung, lymphoid, oesophagus, ovary, pancreas, skin, soft tissue and thyroid. Since tumours are commonly associated with enhanced cell proliferation, we examined the possible correlation of Ki67 and SEPT9 expression in normal tissues and tumours. Our data indicate that the overexpression of SEPT9 in neoplasia is not simply a proliferation-associated phenomenon, despite its role in cytokinesis.

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Acknowledgements

We gratefully acknowledge financial support from the Northern Ireland Research & Development Office, Pathological Society of Great Britain & Ireland and Queen's University Belfast. We thank Adrian Jubb for assistance with data mining and Dr Simon McDade for Figure 1a.

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Correspondence to Peter A Hall.

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Supplementary Information accompanies the paper on Oncogene website (http://www.nature.com/onc)

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Scott, M., Hyland, P., McGregor, G. et al. Multimodality expression profiling shows SEPT9 to be overexpressed in a wide range of human tumours. Oncogene 24, 4688–4700 (2005). https://doi.org/10.1038/sj.onc.1208574

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  • DOI: https://doi.org/10.1038/sj.onc.1208574

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