Cheng-Nan Wu1, Wen-Shin Chang1,2,3, Liang-Chun Shih2,3,4, Yun-Chi Wang2,3, Hsu-Tung Lee5, Chien-Chih Yu3,6, Zhi-Hong Wang7, Mei-Chin Mong7, Te-Chun Hsia3, Chia-Wen Tsai1,2,3, DA-Tian Bau8,3,9. 1. Department of Medical Laboratory Science and Biotechnology, Central Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. 2. Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C. 3. Terry Fox Cancer Research Laboratory, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan, R.O.C. 4. Department of Otorhinolaryngology, China Medical University Hospital, Taichung, Taiwan, R.O.C. 5. Cancer Prevention Center, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C. 6. School of Pharmacy, China Medical University, Taichung, Taiwan, R.O.C. 7. Department of Food Nutrition and Health Biotechnology, Asia University, Taichung, Taiwan, R.O.C. 8. Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C.; datian@mail.cmuh.org.tw artbau2@gmail.com. 9. Department of Bioinformatics and Medical Engineering, Asia University, Taichung, Taiwan, R.O.C.
Abstract
BACKGROUND/AIM: Xeroderma pigmentosum complementation group C (XPC) is reported to play important roles in DNA integrity and genomic instability, however, the contribution of XPC to oral carcinogenesis is largely uncertain. Therefore, we aimed at examining the contribution of XPC genotypes to oral cancer. MATERIALS AND METHODS: The genotypes of XPC rs2228001 and rs2228000 were examined among 958 oral cancer patients and 958 control subjects by polymerase chain reaction-restriction fragment length polymorphism methodology and corresponding DNA repair capacity was checked. RESULTS: First, the percentages of XPC rs2228001 AC and CC were higher among oral cancer patients than controls. Second, no significant association was observed regarding XPC rs2228000. Third, there was a synergistic influence of smoking and betel quid chewing behaviors and XPC rs2228001 genotype on oral cancer risk. Last, functional experiments showed DNA repair capacity was lower for AC/CC carriers than AA carriers. CONCLUSION: XPC rs2228001 C allele, which was associated with decreased DNA repair capacity, may interact with smoking and betel quid chewing behaviors on oral cancer risk. Copyright
BACKGROUND/AIM: Xeroderma pigmentosum complementation group C (XPC) is reported to play important roles in DNA integrity and genomic instability, however, the contribution of XPC to oral carcinogenesis is largely uncertain. Therefore, we aimed at examining the contribution of XPC genotypes to oral cancer. MATERIALS AND METHODS: The genotypes of XPCrs2228001 and rs2228000 were examined among 958 oral cancerpatients and 958 control subjects by polymerase chain reaction-restriction fragment length polymorphism methodology and corresponding DNA repair capacity was checked. RESULTS: First, the percentages of XPCrs2228001 AC and CC were higher among oral cancerpatients than controls. Second, no significant association was observed regarding XPCrs2228000. Third, there was a synergistic influence of smoking and betel quid chewing behaviors and XPCrs2228001 genotype on oral cancer risk. Last, functional experiments showed DNA repair capacity was lower for AC/CC carriers than AA carriers. CONCLUSION:XPCrs2228001 C allele, which was associated with decreased DNA repair capacity, may interact with smoking and betel quid chewing behaviors on oral cancer risk. Copyright