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Head and neck cancer ranks as the seventh most prevalent cancer globally. Radiotherapy is a cornerstone of treatment for patients with this cancer, favored for its high effectiveness and non-invasive nature. Many solid tumors, including those in head and neck cancers, experience areas of permanent or temporary hypoxia due to disrupted blood supply. The tumor hypoxia is a key factor in resistance to radiation therapy, primarily because it decreases reactive oxygen species production, which is crucial for radiation-induced DNA damage. This study aimed to explore how hypoxia affects cell growth, viability, and cytokine production in response to radiation in head and neck cancer cells. In this research, FaDu, Detroit 562 and 2A3 cells were cultured under normal oxygen levels (21% O2) or hypoxic conditions (1% O2) before being exposed to either 0 or 6 Gy of gamma rays from Cobalt-60. Post-irradiation, the cells were examined using flow cytometry to assess survival and proliferation, while cytokine levels in the conditioned media were detected using a cytokine array and quantified through ELISA (IL-8). The findings revealed that hypoxia significantly reduced cancer cells proliferation and altered their survival following radiation exposure. The production of IL-8 chemokine in response to hypoxia and irradiation vary between the three cancer cell lines tested. In FaDu cells, hypoxia, alone or combined with radiation, affected the levels of several cytokines, including SerpinE1/PAI-1, CCL5/RANTES, and CXCL8/IL-8. Additionally, the expression of programmed death-ligand 1 (PD-L1) significantly increased under hypoxia, with or without radiation exposure. The results indicate that hypoxia can modify cancer cells response to radiation. The increased expression of PD-L1 and the chemokine IL-8 suggests that hypoxia might have immunomodulatory effects on the tumor milieu. Understanding the molecular mechanisms and cell signaling within the tumor microenvironment is crucial for developing more effective cancer therapies. This work was supported by the MŠMT grant LUC23033.
