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Mcp-1 Pathway
Annals of Oncology 25 (Supplement 5): v75–v109, 2014 doi:10.1093/annonc/mdu436.8
Poster Session (Poster presentations categorized by each organ) P1
3
5
Chang-Han Chen, Chun-Chieh Yu, Hsin-Ting Tsai Center for Translational Research in Biomedical Sciences, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung Taiwan
abstracts
Head and neck squamous cell carcinoma (HNSCC) is one of the tumors of poor prognosis despite the therapeutic advances in the past few years. It has been reported
Downloaded from https://academic.oup.com/annonc/article-abstract/25/suppl_5/v76/2240526 by guest on 24 October 2019
ANGIOTENSIN II TYPE 1 RECEPTOR SIGNALING PROMOTES HEAD AND NECK CANCER CELLS INVASIVE BEHAVIOR BY FLJ10540/MCP-1 PATHWAY
that overexpression of AT1R occurs in many human carcinomas. However, the molecular mechanisms by which angiotensin II type 1 receptor (AT1R) mediate its invasive effects in HNSCC still unclear. Here, we found that AT1R was not only found in HNSCC specimens, but also significantly correlated with advanced TNM-stage and the poor 5-year survival rate. Thus indicated that AT1R was an independent factor for HNSCC development. Functionally, AT1R could promote tumor growth in nude mice. In addition, AT1R had the abilities to stimulate cell migration and invasion in oral cancer cells through increased FLJ10540 and MCP-1 expression by Transwell chambers. Conversely, depletion of AT1R expression by siRNAs suppressed FLJ10540 and MCP-1 protein expressions. Suppression MCP-1 could cause significant inhibition on cell migratory and invasive ability of AT1R-overexpressing head and neck cancer cells. Finally, immunohistochemical and Western blotting analysis of human aggressive HNSCC specimens showed a significant positively correlation among AT1R, FLJ10540 and MCP-1 expression. These findings suggest that AT1R is not only an important prognostic factor but also a new therapeutic target in the FLJ10540/MCP-1 pathway for HNSCC treatment.
© The Author 2014. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: [email protected].
Poster Session (Poster presentations categorized by each organ) P1
3
5
Chang-Han Chen, Chun-Chieh Yu, Hsin-Ting Tsai Center for Translational Research in Biomedical Sciences, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung Taiwan
abstracts
Head and neck squamous cell carcinoma (HNSCC) is one of the tumors of poor prognosis despite the therapeutic advances in the past few years. It has been reported
Downloaded from https://academic.oup.com/annonc/article-abstract/25/suppl_5/v76/2240526 by guest on 24 October 2019
ANGIOTENSIN II TYPE 1 RECEPTOR SIGNALING PROMOTES HEAD AND NECK CANCER CELLS INVASIVE BEHAVIOR BY FLJ10540/MCP-1 PATHWAY
that overexpression of AT1R occurs in many human carcinomas. However, the molecular mechanisms by which angiotensin II type 1 receptor (AT1R) mediate its invasive effects in HNSCC still unclear. Here, we found that AT1R was not only found in HNSCC specimens, but also significantly correlated with advanced TNM-stage and the poor 5-year survival rate. Thus indicated that AT1R was an independent factor for HNSCC development. Functionally, AT1R could promote tumor growth in nude mice. In addition, AT1R had the abilities to stimulate cell migration and invasion in oral cancer cells through increased FLJ10540 and MCP-1 expression by Transwell chambers. Conversely, depletion of AT1R expression by siRNAs suppressed FLJ10540 and MCP-1 protein expressions. Suppression MCP-1 could cause significant inhibition on cell migratory and invasive ability of AT1R-overexpressing head and neck cancer cells. Finally, immunohistochemical and Western blotting analysis of human aggressive HNSCC specimens showed a significant positively correlation among AT1R, FLJ10540 and MCP-1 expression. These findings suggest that AT1R is not only an important prognostic factor but also a new therapeutic target in the FLJ10540/MCP-1 pathway for HNSCC treatment.
© The Author 2014. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: [email protected].