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Open Access Research article

Opposing function of MYBBP1A in proliferation and migration of head and neck squamous cell carcinoma cells

Gustavo A Acuña Sanhueza123, Leonie Faller1, Babitha George1, Jennifer Koffler1, Vinko Misetic1, Christa Flechtenmacher4, Gerhard Dyckhoff1, Peter P Plinkert1, Peter Angel3, Christian Simon1 and Jochen Hess12*

  • * Corresponding author: Jochen Hess j.hess@dkfz.de

  • † Equal contributors

Author affiliations

1 Department of Otolaryngology, Head and Neck Surgery, University Hospital Heidelberg, 69120 Heidelberg, Germany

2 Junior Research Group Molecular Mechanisms of Head and Neck Tumors, German Cancer Research Center (DKFZ), DKFZ-ZMBH Alliance, 69120 Heidelberg, Germany

3 Division of Signal Transduction and Growth Control, German Cancer Research Center (DKFZ), DKFZ-ZMBH Alliance, 69120 Heidelberg, Germany

4 Institute of Pathology, University Hospital Heidelberg, 69120 Heidelberg, Germany

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Citation and License

BMC Cancer 2012, 12:72  doi:10.1186/1471-2407-12-72

Published: 17 February 2012

Abstract

Background

Head and neck squamous cell carcinoma (HNSCC) is one of the most prevalent and lethal cancers worldwide and mortality mostly results from loco-regional recurrence and metastasis. Despite its significance, our knowledge on molecular, cellular and environmental mechanisms that drive disease pathogenesis remains largely elusive, and there are limited therapeutic options, with only negligible clinical benefit.

Methods

We applied global gene expression profiling with samples derived from a recently established mouse model for oral cancer recurrence and identified a list of genes with differential expression between primary and recurrent tumors.

Results

One differentially expressed gene codes for Myb-binding protein 1a (MYBBP1A), which is known as a transcriptional co-regulator that physically interacts with nuclear transcription factors, such as NFκB and p53. We confirmed significantly reduced MYBBP1A protein levels on tissue sections of recurrent mouse tumors compared to primary tumors by immunohistochemistry, and found aberrant MYBBP1A protein levels also in tumor samples of HNSCC patients. Interestingly, silencing of MYBBP1A expression in murine SCC7 and in human HNSCC cell lines elicited increased migration but decreased cell growth.

Conclusion

We provide experimental evidence that MYBBP1A is an important molecular switch in the regulation of tumor cell proliferation versus migration in HNSCC and it will be a major challenge for the future to proof the concept whether regulation MYBBP1A expression and/or function could serve as a novel option for anti-cancer therapy.