Oral surgery, oral medicine, oral pathology and oral radiology · 2015
Effects of human Dachshund homolog 1 on the proliferation, migration, and adhesion of squamous cell carcinoma of the tongue.
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Zhang Li, Wang Cheng-Qin, Liu Fen, Dong Zuo-Qing, Zhao Peng, Dong Xian-Ning, Wei Fengcai, Qu Xun, Xiang Feng-Gang
Аннотация
OBJECTIVE: To investigate the expression and role of human Dachshund homolog 1 (DACH1) in the tongue squamous cell carcinoma (TSCC).
STUDY DESIGN: To explore the expression, regulation, and mechanism of DACH1 in TSCC, nine samples of fresh tumor and adjacent tissues, 51 samples of paraffin-embedded TSCC and paired adjacent tissues, and TSCC cell line SCC-25 were examined. Immunohistochemistry, real-time polymerase chain reaction, Western blot, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, colony formation, Transwell, adhesion assays, and flow cytometry were used.
RESULTS: The DACH1 expression level was significantly lower in tumors than in the adjacent tissues, and such low expression was associated with poor differentiation of tumors, late clinical stage, and lymph node metastasis. Moreover, overexpression of DACH1 might promote apoptosis and inhibit the proliferation, migration, and adhesion of SCC-25 cells.
CONCLUSIONS: DACH1 may be a potential molecular target for the therapy of recurrent and metastatic TSCC.
STUDY DESIGN: To explore the expression, regulation, and mechanism of DACH1 in TSCC, nine samples of fresh tumor and adjacent tissues, 51 samples of paraffin-embedded TSCC and paired adjacent tissues, and TSCC cell line SCC-25 were examined. Immunohistochemistry, real-time polymerase chain reaction, Western blot, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, colony formation, Transwell, adhesion assays, and flow cytometry were used.
RESULTS: The DACH1 expression level was significantly lower in tumors than in the adjacent tissues, and such low expression was associated with poor differentiation of tumors, late clinical stage, and lymph node metastasis. Moreover, overexpression of DACH1 might promote apoptosis and inhibit the proliferation, migration, and adhesion of SCC-25 cells.
CONCLUSIONS: DACH1 may be a potential molecular target for the therapy of recurrent and metastatic TSCC.