%0 Journal Article %T Involvement of Circulating Cell-Free Mitochondrial DNA and Proinflammatory Cytokines in Pathogenesis of Chronic Obstructive Pulmonary Disease and Lung Cancer %J Asian Pacific Journal of Cancer Prevention %I West Asia Organization for Cancer Prevention (WAOCP), APOCP's West Asia Chapter. %Z 1513-7368 %A Bulgakova, Olga %A Kausbekova, Asemgul %A Kussainova, Assiya %A Kalibekov, Nurtas %A Serikbaiuly, Dulat %A Bersimbaev, Rakhmetkazhi %D 2021 %\ 06/01/2021 %V 22 %N 6 %P 1927-1933 %! Involvement of Circulating Cell-Free Mitochondrial DNA and Proinflammatory Cytokines in Pathogenesis of Chronic Obstructive Pulmonary Disease and Lung Cancer %K circulating cell-free mitochondrial DNA %K chronic obstructive pulmonary disease %K Lung cancer %K Interleukin-6 %K diagnostic and prognostic biomarkers %R 10.31557/APJCP.2021.22.6.1927 %X Objective: Circulating cell-free mitochondrial DNA (cf-MtDNA) has been reported in patients with chronic obstructive pulmonary disease (COPD) and lung cancers. However, inter-relationships among the three biological events have not been well-characterized. Therefore, our investigation was conducted to better understand the role of cf-MtDNA on pathogenesis of the two diseases. Methods: Plasma samples were collected from 64 non-small cell lung cancer (NSCLC) patients (before therapy), 45 patients with COPD and 62 healthy individuals. cf-MtDNA copy numbers were detected using quantitative real-time polymerase chain reaction (qRT-PCR) and cytokines were determined using a human ELISA kit. Results: Our data indicate that smoking statuses of the patients and controls were significantly associated with increased cf-MtDNA in plasma samples. Furthermore, NSCLC patients had significantly higher cf-MtDNA copy numbers than COPD patients (p < 0.03) and normal controls (p < 0.02), together with elevated proinflammatory cytokines over the controls (p < 0.05). Our  study shows that the copy numbers for the NSCLC patients were positively associated with their subsequent metastasis but inversely associated with their overall survival.  Conclusion: Our study indicates certain lung injury (e.g., from cigarette smoking) was responsible for the release of cf-MtDNA and proinflammatory cytokines into plasmas among our patients and controls. The increase in cf-MtDNA copy numbers was significantly associated with the development of both COPD and NSCLC, with increase in interleukin 6, and from our 5-year follow-up, with poor prognosis among the NSCLC patients. Therefore, with further validation, cf-MtDNA can be considered for use as diagnostic and prognostic biomarkers for NSCLC. %U https://journal.waocp.org/article_89647_945729a93d3ff239c60debc714220b84.pdf