Abundant hypermethylation of SOCS-1 in clinically silent pituitary adenomas

Buslei, R., Kreutzer, J., Hofmann, B., Schmidt, V., Siebzehnrubl, Florian ORCID: https://orcid.org/0000-0001-8411-8775, Hahnen, E., Eyupoglu, I. Y., Fahlbusch, R. and Blumcke, I. 2006. Abundant hypermethylation of SOCS-1 in clinically silent pituitary adenomas. Acta Neuropathologica 111 (3) , pp. 264-271. 10.1007/s00401-005-0009-9

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Abstract

Janus kinase (JAK)/signal transducers and activators of transcription (STAT) cascade are required for cytokines, growth factors, G-proteins and hormones (growth hormone and prolactin). Gatekeepers in this pathway are the suppressor of cytokine signalling (SOCS) family of proteins. Their expression level is epigenetically regulated by DNA methylation. We have investigated the CpG island methylation status of SOCS-1 in a cohort of pituitary adenomas (PA; n=57), craniopharyngiomas (CP; n=30) and normal pituitary tissue (NP; n=11) using methylation sensitive single-strand conformation polymorphism analysis (MS-SSCP) and direct sequencing. SOCS-1 hypermethylation was identified in 51% (29/57) of surgical specimens obtained from PA patients. 83% of these tumours were clinically silent. In contrast, no methylation of SOCS-1 was observed in CPs or NPs. Quantitative real-time PCR and western blot analysis confirmed reduced SOCS-1 expression in the majority of pituitary adenomas. The data is compatible with epigenetic silencing of the SOCS-1 gene and constitutive activation of the JAK-STAT pathway in PA. This appears to contribute particularly to those tumours characterized by a hormone-inactive status.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences European Cancer Stem Cell Research Institute (ECSCRI)
Publisher:	Springer
ISSN:	0001-6322
Last Modified:	25 Oct 2022 10:12
URI:	https://orca.cardiff.ac.uk/id/eprint/61407

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