Mao-Hong Huang1, Xiao-Bin Zhang1,2,3,4, Hui-Ling Wang1, Liu-Xia Li1, Yi-Ming Zeng2,3,4, Miao Wang1, Hui-Qing Zeng1. 1. Department of Respiratory Medicine, Zhongshan Hospital, Xiamen University, Xiamen 361004, China. 2. Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, China. 3. The Second Clinical Medical College, Fujian Medical University, Quanzhou 362000, China. 4. Respiratory Medicine Center of Fujian Province, Quanzhou 362000, China.
Abstract
BACKGROUND: As a hallmark of obstructive sleep apnea (OSA), intermittent hypoxia (IH) promotes tumor progress. The high expression of programmed death 1 and programmed death ligand 1 (PD-L1) in tumor leads to immune evasion and subsequently aggravates tumor progress. This study aims to determine the tumor PD-L1 expression under the IH condition. METHODS: A total of 24 C57BL/6J mice were randomly assigned to the normoxia (control, CTL) group and the IH group. Mice in the IH group were subjected to the IH condition for 5 weeks. Lung cancer cells were injected into the flank of each mouse after 1 week of IH exposure. Tumor PD-L1 expression was detected by immunohistochemistry (IHC). Correlation between tumor weight, tumor volume, and expression of PD-L1 was analyzed. RESULTS: Compared to the CTL group, mice in the IH group had a high PD-L1 expression. The IH can enhance the tumor PD-L1 expression. Tumor weight, volume, and HIF-1α levels were closely associated with the PD-L1 expression in the IH group, while dissimilar findings were observed in the CTL group. CONCLUSIONS: The IH enhances tumor PD-L1 expression in OSA mimicking mice. Additional studies are required to clarify the underlying mechanism.
BACKGROUND: As a hallmark of obstructive sleep apnea (OSA), intermittent hypoxia (IH) promotes tumor progress. The high expression of programmed death 1 and programmed death ligand 1 (PD-L1) in tumor leads to immune evasion and subsequently aggravates tumor progress. This study aims to determine the tumor PD-L1 expression under the IH condition. METHODS: A total of 24 C57BL/6J mice were randomly assigned to the normoxia (control, CTL) group and the IH group. Mice in the IH group were subjected to the IH condition for 5 weeks. Lung cancer cells were injected into the flank of each mouse after 1 week of IH exposure. Tumor PD-L1 expression was detected by immunohistochemistry (IHC). Correlation between tumor weight, tumor volume, and expression of PD-L1 was analyzed. RESULTS: Compared to the CTL group, mice in the IH group had a high PD-L1 expression. The IH can enhance the tumor PD-L1 expression. Tumor weight, volume, and HIF-1α levels were closely associated with the PD-L1 expression in the IH group, while dissimilar findings were observed in the CTL group. CONCLUSIONS: The IH enhances tumor PD-L1 expression in OSA mimicking mice. Additional studies are required to clarify the underlying mechanism.
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