Yue-Ju Li1,2, Tse-Hung Huang3, Michael Hsiao4, Been-Ren Lin5, Shih-Jung Cheng6, Cheng-Ning Yang1,2,7, Wei-Ting Lai1, Tai-Sheng Wu1, Jia-Ruei Fan3, Mark Yen-Ping Kuo1,3,6, Cheng-Chi Chang2,3,6. 1. Graduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan. 2. Angiogenesis Research Center, National Taiwan University, Taipei, Taiwan. 3. Graduate Institute of Oral Biology, School of Dentistry, National Taiwan University, Taipei, Taiwan. 4. Genomics Research Center, Academia Sinica, Taipei, Taiwan. 5. Department of Surgery, National Taiwan University Hospital, Taipei, Taiwan. 6. Department of Dentistry, National Taiwan University Hospital, Taipei, Taiwan. 7. Department of Otolaryngology, National Taiwan University Hospital, Taipei, Taiwan.
Abstract
BACKGROUND: Glycolysis machinery regulates cancer cell behavior. However, the roles of these glycolysis enzymes in oral squamous cell carcinoma (OSCC) progression remain unknown. METHODS: Fructose-bisphosphate aldolase C (ALDOC) expression in OSCC patients and cell lines was detected using quantitative real-time polymerase chain reaction (PCR). The functions of ALDOC in migration and invasion were determined using gain and loss of function approaches. An orthotopic OSCC animal model was performed to investigate the effects of ALDOC on metastasis and tumorigenesis in vivo. RESULTS: ALDOC expression is negatively significantly correlated with clinical outcome and cell migration in vitro and in vivo. ALDOC blocks adenosine triphosphate generation and lactate production, and mutation constructs of Arg42 and Lys146 functionally restore ALDOC-inhibited cell migration and invasion. CONCLUSION: ALDOC functions as an OSCC prognosis marker clinically, and suppresses migration and invasion by its catalytic domain of Arg42 and Lys146.
BACKGROUND: Glycolysis machinery regulates cancer cell behavior. However, the roles of these glycolysis enzymes in oral squamous cell carcinoma (OSCC) progression remain unknown. METHODS:Fructose-bisphosphate aldolase C (ALDOC) expression in OSCC patients and cell lines was detected using quantitative real-time polymerase chain reaction (PCR). The functions of ALDOC in migration and invasion were determined using gain and loss of function approaches. An orthotopic OSCC animal model was performed to investigate the effects of ALDOC on metastasis and tumorigenesis in vivo. RESULTS:ALDOC expression is negatively significantly correlated with clinical outcome and cell migration in vitro and in vivo. ALDOC blocks adenosine triphosphate generation and lactate production, and mutation constructs of Arg42 and Lys146 functionally restore ALDOC-inhibited cell migration and invasion. CONCLUSION:ALDOC functions as an OSCC prognosis marker clinically, and suppresses migration and invasion by its catalytic domain of Arg42 and Lys146.
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