Jen-Yang Tang1,2, Chih-Wen Shu3, Chun-Lin Wang4, Sheng-Chieh Wang5, Meng-Yang Chang6, Li-Ching Lin7,8,9, Hsueh-Wei Chang10,11,12,13. 1. Department of Radiation Oncology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University , Kaohsiung , Taiwan. 2. Department of Radiation Oncology, Kaohsiung Medical University Hospital , Kaohsiung , Taiwan. 3. School of Medicine for International Students, I-Shou University , Kaohsiung , Taiwan. 4. Food Industry Research and Development Institute, Bioresource Collection and Research Center , Hsinchu , Taiwan. 5. PhD Program in Life Sciences, College of Life Science, Kaohsiung Medical University , Kaohsiung , Taiwan. 6. Department of Medicinal and Applied Chemistry, Kaohsiung Medical University , Kaohsiung , Taiwan. 7. Department of Radiation Oncology, Chi-Mei Foundation Medical Center , Tainan , Taiwan. 8. School of Medicine, Taipei Medical University , Taipei , Taiwan. 9. Chung Hwa University of Medical Technology , Tainan , Taiwan. 10. Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University , Kaohsiung , Taiwan. 11. Institute of Medical Science and Technology, National Sun Yat-sen University , Kaohsiung , Taiwan. 12. Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University , Kaohsiung , Taiwan. 13. Department of Biomedical Science and Environmental Biology, Kaohsiung Medical University , Kaohsiung , Taiwan.
Abstract
Purpose: This study evaluates the growth inhibiting potential of our previously described sulfonyl chromen-4-ones (CHW09) compound in X-ray irradiated oral cancer cells. Materials and methods: The growth inhibiting effect and mechanism of combined CHW09/X-ray treatment was examined by analyzing cell viability, cell cycle, apoptosis, reactive oxygen species (ROS), and DNA damage. Results: Individual treatments of CHW09 (10 μg/mL) and X-ray irradiation (12 Gy) slightly decreased cell viability of oral cancer Ca9-22 (87.25% and 86.54%) and CAL 27 (80.00% and 74.01%) cells and normal oral HGF-1 cells (92.76% and 87.56%) at 24 h-MTS assay, respectively. In a combined treatment (CHW09/X-ray), the cell viability in Ca9-22 and CAL 27 cells was significantly decreased to 73.48% and 59.07%, whereas HGF-1 cells maintained 84.97% viability in 24 h-MTS assay. For CAL 27 cells, both 72 h-MTS assay and clonogenic assay showed that CHW09/X-ray resulted in more growth inhibition than other treatments. Intracellular ROS levels of CHW09/X-ray were higher than for CHW09, X-ray and control. CHW09/X-ray and X-ray alone had higher G2/M arrest than the control and CHW09 alone. Moreover, flow cytometry and western blotting showed that CHW09/X-ray treatment caused higher apoptosis levels. Levels of H2A histone family member X (γH2AX)-based DNA damage and 8-oxo-2'-deoxyguanosine (8-oxodG)-oxidative DNA damage of CHW09/X-ray were higher than for CHW09, X-ray and control. Conclusion: CHW09/X-ray treatment had additive growth inhibiting effects against X-ray irradiated oral cancer cells, partly attributing to apoptosis and ROS generation.
Purpose: This study evaluates the growth inhibiting potential of our previously described sulfonyl chromen-4-ones (CHW09) compound in X-ray irradiated oral cancer cells. Materials and methods: The growth inhibiting effect and mechanism of combined CHW09/X-ray treatment was examined by analyzing cell viability, cell cycle, apoptosis, reactive oxygen species (ROS), and DNA damage. Results: Individual treatments of CHW09 (10 μg/mL) and X-ray irradiation (12 Gy) slightly decreased cell viability of oral cancerCa9-22 (87.25% and 86.54%) and CAL 27 (80.00% and 74.01%) cells and normal oral HGF-1 cells (92.76% and 87.56%) at 24 h-MTS assay, respectively. In a combined treatment (CHW09/X-ray), the cell viability in Ca9-22 and CAL 27 cells was significantly decreased to 73.48% and 59.07%, whereas HGF-1 cells maintained 84.97% viability in 24 h-MTS assay. For CAL 27 cells, both 72 h-MTS assay and clonogenic assay showed that CHW09/X-ray resulted in more growth inhibition than other treatments. Intracellular ROS levels of CHW09/X-ray were higher than for CHW09, X-ray and control. CHW09/X-ray and X-ray alone had higher G2/M arrest than the control and CHW09 alone. Moreover, flow cytometry and western blotting showed that CHW09/X-ray treatment caused higher apoptosis levels. Levels of H2A histone family member X (γH2AX)-based DNA damage and 8-oxo-2'-deoxyguanosine (8-oxodG)-oxidative DNA damage of CHW09/X-ray were higher than for CHW09, X-ray and control. Conclusion:CHW09/X-ray treatment had additive growth inhibiting effects against X-ray irradiated oral cancer cells, partly attributing to apoptosis and ROS generation.