Mitochondrial Dynamics in Non-Small Cell Lung Cancer.

Autor: Dutkowska A; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Domańska-Senderowska D; Department of Biomedicine and Genetics, Medical University of Lodz, 90-647 Lodz, Poland., Czarnecka-Chrebelska KH; Department of Biomedicine and Genetics, Medical University of Lodz, 90-647 Lodz, Poland., Pikus E; Department of Biomedicine and Genetics, Medical University of Lodz, 90-647 Lodz, Poland., Zielińska A; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Biskup L; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Kołodziejska A; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Madura P; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Możdżan M; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Załuska U; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Zheng E; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Adamczyk E; Department of Biomedicine and Genetics, Medical University of Lodz, 90-647 Lodz, Poland., Kędzia K; Department of Thoracic, General and Oncological Surgery, Medical University of Lodz, 90-647 Lodz, Poland., Wcisło S; Department of Thoracic, General and Oncological Surgery, Medical University of Lodz, 90-647 Lodz, Poland., Wawrzycki M; Department of Thoracic, General and Oncological Surgery, Medical University of Lodz, 90-647 Lodz, Poland., Brzeziańska-Lasota E; Department of Biomedicine and Genetics, Medical University of Lodz, 90-647 Lodz, Poland., Jabłoński S; Department of Thoracic, General and Oncological Surgery, Medical University of Lodz, 90-647 Lodz, Poland., Antczak A; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland., Poznański M; Department of General and Oncological Pulmonology, Medical University of Lodz, 90-647 Lodz, Poland.
Jazyk: angličtina
Zdroj: Cancers [Cancers (Basel)] 2024 Aug 12; Vol. 16 (16). Date of Electronic Publication: 2024 Aug 12.
DOI: 10.3390/cancers16162823
Abstrakt: 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.
Databáze: MEDLINE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje