HP2 Laboratory, INSERM U1030, Grenoble Alpes University, 38000, Grenoble, France.
Grenoble Alpes University Hospital, 38000, Grenoble, France.
Sci Rep. 2022 Jul 28;12(1):12916. doi: 10.1038/s41598-022-15541-8.
The association between obstructive sleep apnea (OSA) and cancer is still debated and data are scarce regarding the link between OSA and breast cancer progression. Since conclusive epidemiological studies require large sample sizes and sufficient duration of exposure before incident cancer occurrence, basic science studies represent the most promising approach to appropriately address the topic. Here we assessed the impact of intermittent hypoxia (IH), the major hallmark of OSA, on the development of breast cancer and explored the specific involvement of the endothelin signaling pathway. Original in vitro and in vivo models were used where 3D-spheroids or cultures of murine 4T1 breast cancer cells were submitted to IH cycles, and nude NMRI mice, orthotopically implanted with 4T1 cells, were submitted to chronic IH exposure before and after implantation. The role of the endothelin-1 in promoting cancer cell development was investigated using the dual endothelin receptor antagonist, macitentan. In vitro exposure to IH significantly increased 4T1 cell proliferation and migration. Meta-analysis of 4 independent in vivo experiments showed that chronic IH exposure promoted tumor growth, assessed by caliper measurement (overall standardized mean difference: 1.00 [0.45-1.55], p < 0.001), bioluminescence imaging (1.65 [0.59-2.71]; p < 0.01) and tumor weight (0.86 [0.31-1.41], p < 0.01), and enhanced metastatic pulmonary expansion (0.77 [0.12-1.42]; p = 0.01). Both in vitro and in vivo tumor-promoting effects of IH were reversed by macitentan. Overall, these findings demonstrate that chronic intermittent hypoxia exposure promotes breast cancer growth and malignancy and that dual endothelin receptor blockade prevents intermittent hypoxia-induced tumor development.
阻塞性睡眠呼吸暂停(OSA)与癌症之间的关联仍存在争议,关于 OSA 与乳腺癌进展之间的联系的数据也很少。由于结论性的流行病学研究需要大样本量和足够长的暴露时间才能发生癌症,因此基础科学研究代表了适当解决该主题的最有前途的方法。在这里,我们评估了间歇性低氧(IH),即 OSA 的主要特征,对乳腺癌发展的影响,并探讨了内皮素信号通路的具体参与。使用原代体外和体内模型,3D 球体或小鼠 4T1 乳腺癌细胞培养物接受 IH 循环,并用 4T1 细胞原位植入的裸鼠在植入前后接受慢性 IH 暴露。使用双重内皮素受体拮抗剂马西替坦研究内皮素-1 在促进癌细胞发展中的作用。体外暴露于 IH 可显著增加 4T1 细胞的增殖和迁移。4 项独立的体内实验的荟萃分析表明,慢性 IH 暴露促进了肿瘤生长,通过卡尺测量(总体标准化均数差:1.00 [0.45-1.55],p<0.001)、生物发光成像(1.65 [0.59-2.71];p<0.01)和肿瘤重量(0.86 [0.31-1.41],p<0.01),并增强了转移性肺扩张(0.77 [0.12-1.42];p=0.01)。IH 在体外和体内的促肿瘤作用均被马西替坦逆转。总之,这些发现表明,慢性间歇性低氧暴露促进乳腺癌生长和恶性转化,双重内皮素受体阻断可防止间歇性低氧诱导的肿瘤发展。