Opposing function of MYBBP1A in proliferation and migration of head and neck squamous cell carcinoma cells
| Autor: | Babitha George, Jennifer Koffler, Peter Plinkert, Jochen Hess, Christian Simon, Gerhard Dyckhoff, Gustavo A Acuña Sanhueza, Christa Flechtenmacher, Vinko Misetic, Peter Angel, Leonie Faller |
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| Rok vydání: | 2011 |
| Předmět: |
Pathology
medicine.medical_specialty Cancer Research Nucleocytoplasmic Transport Proteins Blotting Western Real-Time Polymerase Chain Reaction lcsh:RC254-282 Metastasis Mice Surgical oncology Cell Movement Cell Line Tumor Genetics Medicine Gene silencing Animals Humans Nuclear protein Cell Proliferation Mouth neoplasm business.industry Cell growth Gene Expression Profiling Nuclear Proteins RNA-Binding Proteins medicine.disease lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens Head and neck squamous-cell carcinoma Immunohistochemistry Gene expression profiling DNA-Binding Proteins Disease Models Animal Oncology Cancer research Carcinoma Squamous Cell Mouth Neoplasms Neoplasm Recurrence Local business Transcription Factors Research Article |
| Zdroj: | BMC Cancer BMC Cancer, Vol 12, Iss 1, p 72 (2012) |
| ISSN: | 1471-2407 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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