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Objective Recent studies have demonstrated the pro‐tumour role of CD36 in multiple cancer types. However, its role has not been well elucidated in oral squamous cell carcinoma (OSCC). Here, we aimed to evaluate the role of CD36 in proliferation and migration of OSCC cells. Methods Human OSCC cell lines HSC‐2, HSC‐3, HSC‐4 and Ca9‐22 were assessed for proliferation by staining with the cell proliferation marker Ki‐67. We also assessed migration activity, and the expression of cell adhesion molecules such as E‐cadherin and β‐catenin and platelet‐derived growth factor receptors (PDGFRs) of CD36‐positive cells. Results CD36‐positive cells showed increased expression of Ki‐67 and migration activity compared with CD36‐negative cells. Moreover, CD36‐positive cells showed reduced expression of E‐cadherin and β‐catenin, whereas the expression of PDGFRs increased compared with that in CD36‐negative cells. Conclusions Our results strongly suggest that CD36 has an important role in facilitating the proliferation and migration activity of OSCC cells, indicating its usefulness in the diagnosis of high‐grade tumour and targeted therapy of oral cancer.

Cold atmospheric plasmas (CAPs) have been proposed as a novel therapeutic method for its anti-cancer potential. However, its biological effects in combination with other physical modalities remain elusive. Therefore, this study examined the effects of cold atmospheric helium plasma (He-CAP) in combination with hyperthermia (HT) 42 °C or radiation 5 Gy. Synergistic enhancement in the cell death with HT and an additive enhancement with radiation were observed following He-CAP treatment. The synergistic effects were accompanied by increased intracellular reactive oxygen species (ROS) production. Hydrogen peroxide (H2O2) and superoxide (O2 •–) generation was increased immediately after He-CAP treatment, but fails to initiate cell death process. Interestingly, at late hour’s He-CAP-induced O2 •– generation subsides, however the combined treatment showed sustained increased intracellular O2 •– level, and enhanced cell death than either treatment alone. He-CAP caused marked induction of ROS in the aqueous medium, but He-CAP-induced ROS seems insufficient or not completely incorporated intra-cellularly to activate cell death machinery. The observed synergistic effects were due to the HT effects on membrane fluidity which facilitate the incorporation of He-CAP-induced ROS into the cells, thus results in the enhanced cancer cell death following combined treatment. These findings would be helpful when establishing a therapeutic strategy for CAP in combination with HT or radiation.

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