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SnoN expression is differently regulated in microsatellite unstable compared with microsatellite stable colorectal cancers

June A Chia1, Lisa A Simms1, Sarah-Jane Cozzi1, Joanne Young2, Jeremy R Jass3, Michael D Walsh2, Kevin J Spring1, Barbara A Leggett1 and Vicki LJ Whitehall1*

Author Affiliations

1 The Conjoint Gastroenterology Laboratory, Royal Brisbane and Women's Hospital Foundation Clinical Research Centre and the Queensland Institute of Medical Research, Brisbane, 4029, Australia

2 The Molecular Cancer Epidemiology Laboratory, The Queensland Institute of Medical Research, Brisbane, 4029, Australia

3 The Department of Pathology, McGill University, Montreal, H3A 2B4, Canada

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BMC Cancer 2006, 6:252  doi:10.1186/1471-2407-6-252

Published: 24 October 2006



SnoN is an important regulator of the transforming growth factor beta (TGFβ) signalling pathway and has been shown to exhibit both tumour promotion and suppression activity.


To further explore the role of this complex molecule in colorectal tumorigenesis, we examined 52 paired normal and tumour colorectal specimens stratified by level of microsatellite instability; 18 with high-level microsatellite instability (MSI-H) and 34 microsatellite stable (MSS). SnoN transcript expression was quantitated by real-time PCR and analysed with respect to clinical indicators of prognosis.


Within the MSI-H subgroup, SnoN was commonly either up-regulated (6/18, 33%) or down-regulated (7/18, 39%). A significantly different distribution of SnoN expression was observed in MSS cancers compared with MSI-H (P ≤ 0.001). Whilst 17/34 (50%) of MSS tumours demonstrated up-regulation, none showed down-regulated expression. Within the MSI-H subgroup, up-regulation was significantly correlated with lack of repeat tract mutation in the TGFβRII gene (P ≤ 0.025), suggesting that SnoN is more frequently up-regulated in the presence of functional TGFβ signalling.


Together these data support the notion that SnoN has both oncogenic and tumour suppressive properties depending on other genetic changes within the tumour, and that the MSI-H pathway of colorectal tumorigenesis presents an excellent model for the study of these opposing functions.