Abstract
Abstract Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer in the world. Metastases are resistant to conventional therapies and are responsible for 90% of tumour-related death. Better understanding on the molecular mechanism of metastasis may shed light on prevention and treatment of disease. We have established a systemic cellular model for metastases investigation. The parental SAS cells, a low tumorigenic HNSCC cell line; SASVO3 (VO3) cells, a highly tumorigenic cells derived from SAS; and SASVO3M-1 (M1) and SASVO3M-5 (M5) cells, two lines of pulmonary metastatic cells derived from SASVO3 cells using mice model. Transcriptome analysis revealed that M1 and M5 shared the most similar transcription signature and their common genes were designated common M. The profiles of VO3 and common M were distinct from that of parental SAS. Biological pathway analyses showed the signaling of cell movement such as integrin, RhoA, Cdc42, Rac, and actin polymerization were identified in metastatic cells. Of oncogenic properties, metastatic cells possess increased activities of foci formation, filopodia formation, wound healing, and in vivo pulmonary metastases. Interestingly, metabolism assay revealed that the glycolysis activity was increased in highly tumorigenic VO3 cells compare to parental SAS. Yet it was decreased in metastatic M5 cells compared to VO3 cells. “Reverse Warburg effect," which indicating a lowered glycolysis in tumor cells, has been demonstrated by others in metastatic breast cancer by in situ immunohistochemistry stain. The correlation of metabolism and metastasis of HNSCC cells will be discussed. Citation Format: Pei-Fen Su, Shu-Hao Chang, Chia-Hsin Ho, Wei-Li Huang. Increased Rho GTPase and reduced glycolysis activity in metastatic cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 397. doi:10.1158/1538-7445.AM2013-397
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