gms | German Medical Science

76. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V.

04.05. - 08.05.2005, Erfurt

Aberrant Methylation of SOCS-3 in Head and Neck Carcinomas and its precursor lesions: a new therapeutic approach?

Meeting Abstract

  • corresponding author Weber Anette - ENT Department, University of Leipzig
  • Dietz Andreas - ENT Department, University of Leipzig
  • Hengge Ulrich - Dermatology, University of Düsseldorf
  • Tischoff Iris - Institute of Pathology, University of Leipzig
  • Sommerer Florian - Institute of Pathology, University of Leipzig
  • Markwarth Anette - Institute of Pathology, University of Leipzig
  • Tannapfel Andrea - Institute of Pathology, University of Leipzig

Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie. 76. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e.V.. Erfurt, 04.-08.05.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc05hno467

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hno2005/05hno174.shtml

Veröffentlicht: 22. September 2005

© 2005 Anette et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Aims: This study was performed to elucidate the role of Suppressor of Cytokine Signaling (SOCS)-3 in the tumorigenesis of squamous cell carcinoma of the head and neck (HNSCC) and its precursor lesions.

Methods: After microdissection, promoter methylation of SOCS-3 was studied by using methylation-specific PCR in 94 HNSCC, corresponding normal mucosa, lymph node metastases and 16 high and 21 low grade dysplasias. The presence of SOCS-3 mRNA transcripts was confirmed by semiquantitative real-time PCR, and the SOCS-3 protein was analyzed immunohistochemically.

Results: SOCS-3 hypermethylation was found in 85/94 HNSCC (90%) and in 10/16 high and 9/21 low grade dysplasias. Lymph node metastases exhibited an identical methylation status as the primary tumors. In the cell lines tested, SOCS-3 transcripts increased upon treatment with the demethylation compound 5-aza-2-deoxycytidine. Overexpression of wild type SOCS-3 in carcinoma cells with methylated SOCS-3 resulted in the induction of apoptosis and growth suppression as well as downregulation of STAT3, bcl-2 as well as bcl-x.

Conclusions: Our data suggest, that promoter methylation of SOCS-3 is involved in the carcinogenesis of HNSCC. Due to its involvement in tumor growth, restoration of SOCS-3 may hold treatment potential for HNSCC.