Email updates

Keep up to date with the latest news and content from BMC Cancer and BioMed Central.

Open Access Research article

Down-regulation of transcription elogation factor A (SII) like 4 (TCEAL4) in anaplastic thyroid cancer

Junko Akaishi12, Masamitsu Onda1*, Junichi Okamoto12, Shizuyo Miyamoto1, Mitsuji Nagahama3, Kouichi Ito3, Akira Yoshida4 and Kazuo Shimizu2

Author Affiliations

1 Department of Molecular Biology, Institute of Gerontology, Nippon Medical School, Kanagawa, Japan

2 Department of Second Surgery, Nippon Medical School, Tokyo, Japan

3 Department of Surgery, Ito Hospital, Tokyo, Japan

4 Department of Surgery, Kanagawa Prefectual Cancer Center, Kanagawa, Japan

For all author emails, please log on.

BMC Cancer 2006, 6:260  doi:10.1186/1471-2407-6-260

Published: 1 November 2006

Abstract

Background

Anaplastic thyroid cancer (ATC) is one of the most aggressive human malignancies and appears to arise mainly from transformation of pre-existing differentiated thyroid cancer (DTC). However, the carcinogenic mechanism of anaplastic transformation remains unclear. Previously, we investigated specific genes related to ATC based on gene expression profiling using cDNA microarray analysis. One of these genes, transcription elongation factor A (SII)-like 4 (TCEAL4), encodes a member of the transcription elongation factor A (SII)-like gene family. The detailed function of TCEAL4 has not been described nor has any association between this gene and human cancers been reported previously.

Methods

To investigate the role of TCEAL4 in ATC carcinogenesis, we examined expression levels of TCEAL4 in ACLs as well as in other types of thyroid cancers and normal human tissue.

Results

Expression of TCEAL4 was down-regulated in all 11 ACLs as compared to either normal thyroid tissues or papillary and follicular thyroid cancerous tissues. TCEAL4 was expressed ubiquitously in all normal human tissues tested.

Conclusion

To our knowledge, this is the first report of altered TCEAL4 expression in human cancers. We suggest that loss of TCEAL4 expression might be associated with development of ATC from DTC. Further functional studies are required.