Abstract
Cryptocaryone (CPC) was previously reported as preferential for killing natural products in oral cancer cells. However, its radiosensitizing potential combined with ultraviolet C (UVC) cell killing of oral cancer cells remains unclear. This study evaluates the combined anti-proliferation effect and clarifies the mechanism of combined UVC/CPC effects on oral cancer cells. UVC/CPC shows higher anti-proliferation than individual and control treatments in a low cytotoxic environment on normal oral cells. Mechanistically, combined UVC/CPC generates high levels of reactive oxygen species and induces mitochondrial dysfunction by generating mitochondrial superoxide, increasing mitochondrial mass and causing the potential destruction of the mitochondrial membrane compared to individual treatments. Moreover, combined UVC/CPC causes higher G2/M arrest and triggers apoptosis, with greater evidence of cell cycle disturbance, annexin V, pancaspase, caspases 3/7 expression or activity in oral cancer cells than individual treatments. Western blotting further indicates that UVC/CPC induces overexpression for cleaved types of poly (ADP-ribose) polymerase and caspase 3 more than individual treatments. Additionally, UVC/CPC highly induces γH2AX and 8-hydroxy-2’-deoxyguanosine adducts as DNA damage in oral cancer cells. Taken together, CPC shows a radiosensitizing anti-proliferation effect on UVC irradiated oral cancer cells with combined effects through oxidative stress, apoptosis and DNA damage.
Highlights
Oral cancer is a high morbidity-causing cancer worldwide [1,2], which causes high mortality at the same time [3]
The present study focuses on improving anti-proliferation in oral cancer cells by a combined ultraviolet C (UVC)/CPC treatment
The present study shows that UVC with CPC (UVC/CPC) exhibits higher oxidative stress (ROS and MitoSOX) than a single treatment in oral cancer cells (Figure 2)
Summary
Oral cancer is a high morbidity-causing cancer worldwide [1,2], which causes high mortality at the same time [3]. Oral cancer is highly prevalent in several countries with the increased popularity of betel nut chewing, alcohol consumption, and tobacco smoking [4]. The incidence and death rate of oral cancer increases every year for both genders [5]. It is vital to cure oral cancer by developing more effective treatments. Combined treatment of anticancer agents with radiotherapy is a common strategy in oral cancer therapy [6,7]. This combined treatment commonly shows side effects on normal tissues because of the cytotoxicity of common radiosensitizers. Radiosensitizing agents with a preferential killing ability are expected to reduce side effects on normal cells
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