In lung cancer patients, two complementary abnormalities were found that can cause disruption of the mitochondrial network: increased fusion and impaired fission, manifested by reduced levels of FIS1, a mitochondrial division regulator, and increased expression of MFN1, a mitochondrial fusion mediator. Immunoexpression studies of MFN1 and FIS1 proteins were performed in serum samples obtained from 47 patients with non-small cell lung cancer (NSCLC) and 21 controls. In the NSCLC patients, the immunoexpression of the MFN1 protein was significantly higher, and the FIS1 protein level was significantly lower than in the control group (p< 0.01;p< 0.001; UMW test). Patients with early, operable lung cancer had significantly lower levels of MFN1 immunoexpression compared to patients with advanced, metastatic lung cancer (p< 0.05; UMW test). This suggests that early stages of the disease are characterized by greater fragmentation of damaged mitochondria and apoptosis. In contrast, lower FIS1 protein levels were associated with a worse prognosis. Increased mitochondrial fusion in the blood of lung cancer patients may suggest an increase in protective and repair mechanisms. This opens up questions about why these mechanisms fail in the context of existing advanced cancer disease and is a starting point for further research into why protective mechanisms fail in lung cancer patients.
在肺癌患者中，发现两种可导致线粒体网络紊乱的互补性异常：融合增强与分裂受损，具体表现为线粒体分裂调控因子FIS1水平降低，以及线粒体融合介质MFN1表达升高。研究对47例非小细胞肺癌（NSCLC）患者和21例对照者的血清样本进行了MFN1与FIS1蛋白的免疫表达分析。结果显示，NSCLC患者MFN1蛋白免疫表达水平显著高于对照组，而FIS1蛋白水平显著低于对照组（p<0.01；p<0.001；UMW检验）。早期可手术肺癌患者的MFN1免疫表达水平显著低于晚期转移性肺癌患者（p<0.05；UMW检验），提示疾病早期阶段以受损线粒体碎片化增强及细胞凋亡为特征。相反，FIS1蛋白水平降低与不良预后相关。肺癌患者血液中线粒体融合增强可能意味着保护性与修复机制增强。这引发了对现有晚期癌症背景下这些机制为何失效的思考，并为深入研究肺癌患者保护机制失效原因提供了切入点。
肿瘤(癌症)患者之家