Abstract
Abstract Oral cancer is the sixth leading cancer in the world. Cisplatin is the first-line of chemotherapeutic drug for the treatment of oral cancer, however, cancer with cisplatin resistance is a significant cause of treatment failure. To investigate the mechanism of cisplatin resistance, we established cisplatin-resistant (CR) subline cells from SAS, CGHNC8, and CGHNC9 oral cancer cell lines. The transcriptomic profiling analysis was performed between parental and CR subline cells to global survey and identify cisplatin-resistant genes. Total of 345 genes were differentially expressed in both SAS and CGHNC8 cells, in which 16 genes were confirmed. KCNJ2 was shown highest over-expression in both CR subline cells, and was selected for further investigation. KCNJ2 is a molecular potassium influx channel, which allows potassium flowing into cells to maintain ion homeostasis. To determine potential effect of KCNJ2, we have established KCNJ2 stable knocked down cells. Results showed that KCNJ2 knockdown cells were more sensitive to cisplatin treatment, as demonstrated by significantly reduced potassium influx, accelerated apoptosis by increasing caspase activity, and led to reduced cellular clonogenic survival. Taking together, we have profiled transcriptomes and identified at least 16 genes which may associate with cisplatin resistance in oral cancer cells. KCNJ2 silencing sensitizes cisplatin-resistant cells, through suppression of potassium influx. This study serves as knowledge foundation for clinical application in the prediction or prognosis of cisplatin treatment for oral cancer. Citation Format: Yen Liang Li. Silencing of KCNJ2, a potassium influx channel, increases cisplatin-induced cell death in oral cancer. [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 2119. doi:10.1158/1538-7445.AM2013-2119
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.