【摘 要】
：
In order to find one or more suppressors of tumor progression in vivo for head and neck squamous cell carcinoma (HNSCC), we searched for molecules down-regulated in HNSCC cells when the cells were tre
【机 构】
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Oral Health Science Research Center Kanagawa Dental College Japan
【出 处】
：
BITs 3rd Annual World Cancer Congress-2012(2012第五届世界癌症大会)
论文部分内容阅读
In order to find one or more suppressors of tumor progression in vivo for head and neck squamous cell carcinoma (HNSCC), we searched for molecules down-regulated in HNSCC cells when the cells were treated with epidermal growth factor (EGF), whose receptor is frequently over-activated in HNSCC.The expression of BRAK, which is also known as CXC chemokine ligand14 (CXCL14), was down-regulated significantly by the treatment of HNSCC cells with EGF as observed by cDNA microarray analysis followed by reverse-transcriptase polymerase chain reaction analysis and western blotting.The EGF effect on the expression of CXCL14/BRAK was attenuated by the co-presence of inhibitors of the EGF receptor, or inhibitors of MEK and ERK, down-stream signaling molecules of EGF receptor.The rate of tumor formation in vivo of BRAK-expressing vector-transfected tumor cells in T-cell deficient athymic nude mice or T-and B-cell deficient SCID mice was significantly lower than those of mock vector-transfected ones.Tumors formed in vivo by the BRAK-expressing cells were significantly smaller than those of the mock-transfected ones.In addition transgenic mice over-expressing chemokine CXCL 14/BRAK suppressed growth of tumor cell transplants and suppressed tumor metastasis.These results indicate that BRAK/CXCL14 is a chemokine having suppressive activity toward progression of tumor growth and metastasis in vivo.Our approach will be useful in finding new target molecules to suppress tumor progression.
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