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Original Articles

Sulfonyl chromen-4-ones (CHW09) shows an additive effect to inhibit cell growth of X-ray irradiated oral cancer cells, involving apoptosis and ROS generation

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Pages 1226-1235 | Received 28 Aug 2018, Accepted 12 May 2019, Published online: 17 Jun 2019
 

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.

Acknowledgments

The authors thank our colleague Dr. Hans-Uwe Dahms for editing the manuscript.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was partly supported by funds of the Ministry of Science and Technology [MOST 107-2320-B-037-016, MOST 107-2314-B-037-048, and MOST 107-2311-B-214-003], the National Sun Yat-sen University-KMU Joint Research Project [#NSYSUKMU 108-P001], the Kaohsiung Medical University Hospital [KMUH107-7R74], the Ministry of Economic Affairs [107-EC-17-A-22-0643 and 107-EC-17-A-22-0525], the Chimei-KMU jointed project (108CM-KMU-11), Regenerative Medicine and Cell Therapy Research Center (KMU-TC108A02), and the Health and welfare surcharge of tobacco products, the Ministry of Health and Welfare, Taiwan, Republic of China [MOHW 108-TDU-B-212-124016].

Notes on contributors

Jen-Yang Tang

Jen-Yang Tang, MD/PhD. He is an Attending Physician in Kaohsiung Medical University Hospital and his research field is radiotherapy.

Chih-Wen Shu

Chih-Wen Shu, PhD. His research fields are autophagy and cancer biology.

Chun-Lin Wang

Chun-Lin Wang, MSc in Life Science. He is an Associate researcher in the Food Industry Research and Development Institute, Bioresource Collection and Research Center, Hsinchu, Taiwan.

Sheng-Chieh Wang

Sheng-Chieh Wang, MSc in Seafood Science. He is currently working as a PhD Student in College of Life Science, Kaohsiung Medical University, Taiwan.

Meng-Yang Chang

Meng-Yang Chang, PhD. His research field is organic synthesis for medicinal and clinical compounds.

Li-Ching Lin

Li-Ching Lin, MD. He is Chief, Radiation Oncology, Chi-Mei Foundation Medical Center.

Hsueh-Wei Chang

Hsueh-Wei Chang, PhD. He is dean of College of Life Science, Kaohsiung Medical University. His research fields are anticancer natural products and radiosensitizers.

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