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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">urmj</journal-id><journal-title-group><journal-title xml:lang="ru">Уральский медицинский журнал</journal-title><trans-title-group xml:lang="en"><trans-title>Ural Medical Journal</trans-title></trans-title-group></journal-title-group><issn pub-type="epub">2949-4389</issn><publisher><publisher-name>Ural State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.52420/umj.24.5.50</article-id><article-id custom-type="edn" pub-id-type="custom">MOBCUF</article-id><article-id custom-type="elpub" pub-id-type="custom">urmj-1971</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>Оригинальные статьи | Original articles</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Original articles</subject></subj-group></article-categories><title-group><article-title>Особенности молекулярного взаимодействия карциномы легкого и туберкулеза в эксперименте</article-title><trans-title-group xml:lang="en"><trans-title>Features of Molecular Interaction Between Lung Carcinoma and Tuberculosis In Vivo</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1701-4180</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Агафонов</surname><given-names>Г. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Agafonov</surname><given-names>G. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Агафонов Георгий Михайлович — торакальный хирург, стажер-исследователь, СПб НИИФ.</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Georgiy M. Agafonov — Thoracic Surgeon, Trainee-Researcher, Saint Petersburg State Research Institute of Phthisiopulmonology.</p><p>Saint Petersburg</p></bio><email xlink:type="simple">gm.agafonov@spbniif.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2810-8852</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кудряшов</surname><given-names>Г. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Kudriashov</surname><given-names>G. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кудряшов Григорий Геннадьевич — кандидат медицинских наук, ведущий научный сотрудник, руководитель отдела пульмонологии и торакальной хирургии.</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Grigorii G. Kudriashov — Candidate of Sciences (Medicine), Leading Researcher, Head of the Department of Pulmonology and Thoracic Surgery, Saint Petersburg State Research Institute of Phthisiopulmonology.</p><p>Saint Petersburg</p></bio><email xlink:type="simple">dr.kudriashov.gg@yandex.com</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8698-7904</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Крылова</surname><given-names>Ю. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Krylova</surname><given-names>J. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Крылова Юлия Сергеевна — кандидат медицинских наук, патологоанатом, старший научный сотрудник центра молекулярной биомедицины.</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Julia S. Krylova — Candidate of Sciences (Medicine), Pathologist, Senior Researcher of the Center of Molecular Biomedicine, Saint Petersburg State Research Institute of Phthisiopulmonology.</p><p>Saint Petersburg</p></bio><email xlink:type="simple">info@spbniif.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9518-2916</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Зубарева</surname><given-names>Т. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Zubareva</surname><given-names>T. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Зубарева Татьяна Станиславовна — кандидат биологических наук, старший научный сотрудник центра молекулярной биомедицины.</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Tatiana S. Zubareva — Candidate of Sciences (Biology), Senior Researcher of the Center of Molecular Biomedicine, Saint Petersburg State Research Institute of Phthisiopulmonology.</p><p>Saint Petersburg</p></bio><email xlink:type="simple">tz6.6@bk.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7302-5581</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кветной</surname><given-names>И. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Kvetnoy</surname><given-names>I. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кветной Игорь Моисеевич — доктор медицинских наук, профессор, руководитель Центра молекулярной биомедицины, СПб НИИФ; профессор кафедры патологии, медицинский институт, СПбГУ.</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Igor M. Kvetnoy — Doctor of Sciences (Medicine), Professor, Head of the Center of Molecular Biomedicine, Saint Petersburg State Research Institute of Phthisiopulmonology; Professor of the Department of Pathology, Institute of Medicine, Saint Petersburg State University.</p><p>Saint Petersburg</p></bio><email xlink:type="simple">igor.kvetnoy@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-4385-9643</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Яблонский</surname><given-names>П. К.</given-names></name><name name-style="western" xml:lang="en"><surname>Yablonskiy</surname><given-names>P. K.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Яблонский Пётр Казимирович — доктор медицинских наук, профессор, директор, СПб НИИФ; заведующий кафедрой госпитальной хирургии, медицинский институт, СПбГУ.</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Piotr K. Yablonskii — Doctor of Sciences (Medicine), Professor, Director, Saint-Petersburg State Research Institute of Phthisiopulmonology; Head of the Department of Hospital Surgery, Institute of Medicine, Saint Petersburg State University.</p><p>Saint Petersburg</p></bio><email xlink:type="simple">glhirurgb2@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Санкт-Петербургский научно-исследовательский институт фтизиопульмонологии; Санкт-Петербургский государственный университет</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Saint Petersburg State Research Institute of Phthisiopulmonology; Saint Petersburg State University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Санкт-Петербургский научно-исследовательский институт фтизиопульмонологии</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Saint Petersburg State Research Institute of Phthisiopulmonology</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>02</day><month>11</month><year>2025</year></pub-date><volume>24</volume><issue>5</issue><elocation-id>50–63</elocation-id><permissions><copyright-statement>Copyright &amp;#x00A9; Агафонов Г.М., Кудряшов Г.Г., Крылова Ю.С., Зубарева Т.С., Кветной И.М., Яблонский П.К., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Агафонов Г.М., Кудряшов Г.Г., Крылова Ю.С., Зубарева Т.С., Кветной И.М., Яблонский П.К.</copyright-holder><copyright-holder xml:lang="en">Agafonov G.M., Kudriashov G.G., Krylova J.S., Zubareva T.S., Kvetnoy I.M., Yablonskiy P.K.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.umjusmu.ru/jour/article/view/1971">https://www.umjusmu.ru/jour/article/view/1971</self-uri><abstract><sec><title>Введение</title><p>Введение. Рак легкого и туберкулез возглавляют список социально значимых болезней во всем мире. Основы взаимодействия двух патологических процессов в настоящий момент до конца не изучены.</p><p>Цель исследования — изучить влияние туберкулеза легких на развитие злокачественной опухоли легкого.</p></sec><sec><title>Материалы и методы</title><p>Материалы и методы. Использована модель (патент RU 2800964 C1) эпидермоидной опухоли Льюис (LLC) и генерализованного туберкулеза (штаммы H37Rv и 5582) мышей линии C57BL/6. Сформировано 5 групп лабораторных животных: изолированный туберкулез (с различной чувствительностью), изолированная LLC и 2 группы сочетанной патологии с различной чувствительностью M. tuberculosis. Выполнено иммуногистохимическое исследование образцов легкого с определением относительной экспрессии TNF-α, PCNA и MMP-9.</p></sec><sec><title>Результаты</title><p>Результаты. Относительная экспрессия MMP-9 в группах сочетанной патологии статистически значимо ниже, чем в группе изолированной опухоли: LLC + H37Rv — 2,60; LLC + 5582–3,00; LLC — 8,90 (p = 0,043). Относительная экспрессия TNF-α не имела статистически значимых различий при сравнении групп сочетанной патологии и изолированной опухоли: LLC + H37Rv — 1,35; LLC + 5582–3,70; LLC — 1,70. Статистически значимо более высокий показатель экспрессии TNF-α наблюдался в группах мышей, инфицированных штаммом M. tuberculosis 5582. Относительная экспрессия PCNA статистически значимо ниже при сравнении групп сочетанной патологии и изолированной опухоли: LLC + H37Rv — 8,50; LLC + 5582–14,30; LLC — 36,45 (p = 0,012).</p></sec><sec><title>Обсуждение</title><p>Обсуждение. Полученные данные продемонстрировали, что инфицирование мышей с LLC штаммами M. tuberculosis приводит к подавлению опухоль-индуцированной экспрессии MMP-9 и снижению экспрессии PCNA, что может указывать на подавление процессов метастазирования и пролиферации опухолевых клеток. Уровень экспрессии TNF-α значимо не различался между группами, что не позволило сделать предположение о его влиянии на течение сочетанной патологии.</p></sec><sec><title>Заключение</title><p>Заключение. Полученные данные могут свидетельствовать об онкосупрессивном влиянии туберкулеза легких на развитие опухоли легкого.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction. The mechanisms of interaction between lung cancer and tuberculosis (TB) are not fully understood.</p><p>The aim of the study is to study the effect of pulmonary tuberculosis on the lung cancer.</p></sec><sec><title>Materials and methods</title><p>Materials and methods. The study utilized a model (Patent RU 2800964 C1) of isolated Lewis lung carcinoma (LLC) and generalized TB (H37Rv and 5582 strains) in C57BL/6 mice. Five groups of laboratory animals were formed: isolated tuberculosis (different M. tuberculosis susceptibility), isolated LLC, and 2 groups with combined pathology. An immunohistochemical analysis for TNF-α, PCNA, and MMP-9 was completed.</p></sec><sec><title>Results</title><p>Results. The relative expression of MMP-9 in the groups with combined pathology was significantly lower than in the isolated tumor group: LLC + H37Rv — 2.60; LLC + 5582–3.00; LLC — 8.90 (p = 0.043). The relative expression of TNF-α showed no statistically significant differences between the combined pathology groups and the isolated tumor group: LLC + H37Rv — 1.35; LLC + 5582–3.70; LLC — 1.70. A statistically significant increase in TNF-α expression was observed in mice infected with the drug-resistant M. tuberculosis strain (5582). The relative expression of PCNA was significantly lower in the combined pathology groups compared to the isolated tumor group: LLC + H37Rv — 8.50; LLC + 5582 — 14.30; LLC — 36.45 (p = 0.012).</p></sec><sec><title>Discussion</title><p>Discussion. Data demonstrated that TB led to the suppression of tumor-induced MMP-9 expression, reduction in PCNA expression. This may indicate the suppression of metastasisе, cell proliferation. The TNF-α expression level didn`t differ significantly between the groups.</p></sec><sec><title>Conclusion</title><p>Conclusion. The obtained data may suggest an oncosuppressive effect of tuberculosis on the lung tumors.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>рак легкого</kwd><kwd>туберкулез</kwd><kwd>сочетание рака легкого и туберкулеза</kwd><kwd>иммуногистохимическое исследование</kwd><kwd>TNF-α</kwd><kwd>MMP-9</kwd><kwd>PCNA</kwd></kwd-group><kwd-group xml:lang="en"><kwd>lung cancer</kwd><kwd>tuberculosis</kwd><kwd>concomitant lung cacner and tuberculosis</kwd><kwd>immunohistochemistry</kwd><kwd>TNF-α</kwd><kwd>MMP-9</kwd><kwd>PCNA</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Bray F, Laversanne M, Sung H, Ferlay J, Siegel RL, Soerjomataram I, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA: A Cancer Journal for Clinicians. 2024;74(3):229–263. DOI: https://doi.org/10.3322/caac.21834.</mixed-citation><mixed-citation xml:lang="en">Bray F, Laversanne M, Sung H, Ferlay J, Siegel RL, Soerjomataram I, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA: A Cancer Journal for Clinicians. 2024;74(3):229–263. DOI: https://doi.org/10.3322/caac.21834.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Kudriashov GG, Nefedov AO, Tochilnikov GV, Zmitrichenko YG, Krylova YS, Dogonadze MZ, et al. Original experimental model of tuberculosis and lung cancer. Pediatrician. 2022;13(5):33–42. DOI: https://doi.org/10.17816/PED13533-42.</mixed-citation><mixed-citation xml:lang="en">Kudriashov GG, Nefedov AO, Tochilnikov GV, Zmitrichenko YG, Krylova YS, Dogonadze MZ, et al. Original experimental model of tuberculosis and lung cancer. Pediatrician. 2022;13(5):33–42. DOI: https://doi.org/10.17816/PED13533-42.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Krylova YuS, Kudriashov GG, Tochilnikov GV, Vinogradova TI, Dokhov MA, Yablonskiy PK. Biological model of lung cancer combination and tuberculosis: Development for preclinical study of rational combinations of targeted antitumor and antituberculosis therapy. Molecular Medicine. 2024;22(2):23–28. (In Russ.). DOI: https://doi.org/10.29296/24999490-2024-02-04.</mixed-citation><mixed-citation xml:lang="en">Krylova YuS, Kudriashov GG, Tochilnikov GV, Vinogradova TI, Dokhov MA, Yablonskiy PK. Biological model of lung cancer combination and tuberculosis: Development for preclinical study of rational combinations of targeted antitumor and antituberculosis therapy. Molecular Medicine. 2024;22(2):23–28. (In Russ.). DOI: https://doi.org/10.29296/24999490-2024-02-04.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Zhou Y, Hu Z, Cao S, Yan B, Qian J, Zhong H. Concomitant Mycobacterium tuberculosis infection promotes lung tumor growth through enhancing Treg development. Oncology Reports. 2017;38(2):685–692. DOI: https://doi.org/10.3892/or.2017.5733.</mixed-citation><mixed-citation xml:lang="en">Zhou Y, Hu Z, Cao S, Yan B, Qian J, Zhong H. Concomitant Mycobacterium tuberculosis infection promotes lung tumor growth through enhancing Treg development. Oncology Reports. 2017;38(2):685–692. DOI: https://doi.org/10.3892/or.2017.5733.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Ziółkowska-Suchanek I, Żurawek M. FOXP3: A player of immunogenetic architecture in lung cancer. Genes. 2024;15(4):493. DOI: https://doi.org/10.3390/genes15040493.</mixed-citation><mixed-citation xml:lang="en">Ziółkowska-Suchanek I, Żurawek M. FOXP3: A player of immunogenetic architecture in lung cancer. Genes. 2024;15(4):493. DOI: https://doi.org/10.3390/genes15040493.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Agafonov GM, Kudriashov GG, Krylova YuS, Zubareva TS, Kvetnoy IM, Yablonskiy PK. Lung cancer and pulmonary tuberculosis: Key features of molecular mechanisms of concomitant disease. Progress in Physiological Science. 2024;55(3):58–74. (In Russ.). DOI: https://doi.org/10.31857/S0301179824030045.</mixed-citation><mixed-citation xml:lang="en">Agafonov GM, Kudriashov GG, Krylova YuS, Zubareva TS, Kvetnoy IM, Yablonskiy PK. Lung cancer and pulmonary tuberculosis: Key features of molecular mechanisms of concomitant disease. Progress in Physiological Science. 2024;55(3):58–74. (In Russ.). DOI: https://doi.org/10.31857/S0301179824030045.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Niland S, Riscanevo AX, Eble JA. Matrix metalloproteinases shape the tumor microenvironment in cancer progression. International Journal of Molecular Sciences. 2022;23(1):146. DOI: https://doi.org/10.3390/ijms23010146.</mixed-citation><mixed-citation xml:lang="en">Niland S, Riscanevo AX, Eble JA. Matrix metalloproteinases shape the tumor microenvironment in cancer progression. International Journal of Molecular Sciences. 2022;23(1):146. DOI: https://doi.org/10.3390/ijms23010146.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Quintero-Fabián S, Arreola R, Becerril-Villanueva E, Torres-Romero JC, Arana-Argáez V, Lara-Riegos J, et al. Role of matrix metalloproteinases in angiogenesis and cancer. Frontiers in Oncology. 2019;9:01370. DOI: https://doi.org/10.3389/fonc.2019.01370.</mixed-citation><mixed-citation xml:lang="en">Quintero-Fabián S, Arreola R, Becerril-Villanueva E, Torres-Romero JC, Arana-Argáez V, Lara-Riegos J, et al. Role of matrix metalloproteinases in angiogenesis and cancer. Frontiers in Oncology. 2019;9:01370. DOI: https://doi.org/10.3389/fonc.2019.01370.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Farina AR, Mackay AR. Gelatinase B/MMP-9 in tumour pathogenesis and progression. Cancers. 2014; 6(1):240–296. DOI: https://doi.org/10.3390/cancers6010240.</mixed-citation><mixed-citation xml:lang="en">Farina AR, Mackay AR. Gelatinase B/MMP-9 in tumour pathogenesis and progression. Cancers. 2014; 6(1):240–296. DOI: https://doi.org/10.3390/cancers6010240.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Cabral-Pacheco GA, Garza-Veloz I, Rosa CCD La, Ramirez-Acuña JM, Perez-Romero BA, Guerrero-Rodriguez JF, et al. The roles of matrix metalloproteinases and their inhibitors in human diseases. International Journal of Molecular Sciences. 2020;21(24):9739. DOI: https://doi.org/10.3390/ijms21249739.</mixed-citation><mixed-citation xml:lang="en">Cabral-Pacheco GA, Garza-Veloz I, Rosa CCD La, Ramirez-Acuña JM, Perez-Romero BA, Guerrero-Rodriguez JF, et al. The roles of matrix metalloproteinases and their inhibitors in human diseases. International Journal of Molecular Sciences. 2020;21(24):9739. DOI: https://doi.org/10.3390/ijms21249739.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Shao W, Wang W, Xiong XG, Cao C, Yan TD, Chen G, et al. Prognostic impact of MMP-2 and MMP-9 expression in pathologic stage IA non-small cell lung cancer. Journal of Surgical Oncology. 2011;104(7): 841–846. DOI: https://doi.org/10.1002/jso.22001.</mixed-citation><mixed-citation xml:lang="en">Shao W, Wang W, Xiong XG, Cao C, Yan TD, Chen G, et al. Prognostic impact of MMP-2 and MMP-9 expression in pathologic stage IA non-small cell lung cancer. Journal of Surgical Oncology. 2011;104(7): 841–846. DOI: https://doi.org/10.1002/jso.22001.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang Y, Wu JZ, Zhang JY, Xue J, Ma R, Cao HX, et al. Detection of circulating vascular endothelial growth factor and matrix metalloproteinase-9 in non-small cell lung cancer using Luminex multiplex technology. Oncology Letters. 2014;7(2):499–506. DOI: https://doi.org/10.3892/ol.2013.1718.</mixed-citation><mixed-citation xml:lang="en">Zhang Y, Wu JZ, Zhang JY, Xue J, Ma R, Cao HX, et al. Detection of circulating vascular endothelial growth factor and matrix metalloproteinase-9 in non-small cell lung cancer using Luminex multiplex technology. Oncology Letters. 2014;7(2):499–506. DOI: https://doi.org/10.3892/ol.2013.1718.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Esmedlyaeva DS, Alekseeva NP, Novitskaya TA, Dyakova MYe, Ariel IV, Grigoriev BM, et al. Inflammatory activity and markers of extracellular matrix destruction in pulmonary tuberculoma. Bulletin of Siberian Medicine. 2020;19(2):112–119. DOI: https://doi.org/10.20538/1682-0363-2020-2-112-119.</mixed-citation><mixed-citation xml:lang="en">Esmedlyaeva DS, Alekseeva NP, Novitskaya TA, Dyakova MYe, Ariel IV, Grigoriev BM, et al. Inflammatory activity and markers of extracellular matrix destruction in pulmonary tuberculoma. Bulletin of Siberian Medicine. 2020;19(2):112–119. DOI: https://doi.org/10.20538/1682-0363-2020-2-112-119.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Elkington PT, Ugarte-Gil CA, Friedland JS. Matrix metalloproteinases in tuberculosis. European Respiratory Journal. 2011;38(2);456–464. DOI: https://doi.org/10.1183/09031936.00015411.</mixed-citation><mixed-citation xml:lang="en">Elkington PT, Ugarte-Gil CA, Friedland JS. Matrix metalloproteinases in tuberculosis. European Respiratory Journal. 2011;38(2);456–464. DOI: https://doi.org/10.1183/09031936.00015411.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Ong CWM, Elkington PT, Friedland JS. Tuberculosis, pulmonary cavitation, and matrix metalloproteinases. American Journal of Respiratory and Critical Care Medicine. 2014;190(1):9–18. DOI: https://doi.org/10.1164/rccm.201311-2106PP.</mixed-citation><mixed-citation xml:lang="en">Ong CWM, Elkington PT, Friedland JS. Tuberculosis, pulmonary cavitation, and matrix metalloproteinases. American Journal of Respiratory and Critical Care Medicine. 2014;190(1):9–18. DOI: https://doi.org/10.1164/rccm.201311-2106PP.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Kumar NP, Moideen K, Nancy A, Viswanathan V, Thiruvengadam K, Sivakumar S, et al. Association of plasma matrix metalloproteinase and tissue inhibitors of matrix metalloproteinase levels with adverse treatment outcomes among patients with pulmonary tuberculosis. JAMA Network Open. 2020;3(12):e2027754. DOI: https://doi.org/10.1001/jamanetworkopen.2020.27754.</mixed-citation><mixed-citation xml:lang="en">Kumar NP, Moideen K, Nancy A, Viswanathan V, Thiruvengadam K, Sivakumar S, et al. Association of plasma matrix metalloproteinase and tissue inhibitors of matrix metalloproteinase levels with adverse treatment outcomes among patients with pulmonary tuberculosis. JAMA Network Open. 2020;3(12):e2027754. DOI: https://doi.org/10.1001/jamanetworkopen.2020.27754.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Ordonez AA, Tasneen R, Pokkali S, Xu Z, Converse PJ, Klunk MH, et al. Mouse model of pulmonary cavitary tuberculosis and expression of matrix metalloproteinase-9. Disease Models and Mechanisms. 2016; 9(7):779–788. PMID: https://pubmed.gov/27482816.</mixed-citation><mixed-citation xml:lang="en">Ordonez AA, Tasneen R, Pokkali S, Xu Z, Converse PJ, Klunk MH, et al. Mouse model of pulmonary cavitary tuberculosis and expression of matrix metalloproteinase-9. Disease Models and Mechanisms. 2016; 9(7):779–788. PMID: https://pubmed.gov/27482816.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Rohlwink UK, Walker NF, Ordonez AA, Li YJ, Tucker EW, Elkington PT, et al. Matrix metalloproteinases in pulmonary and central nervous system tuberculosis — a review. International Journal of Molecular Sciences. 2019;20(6):1350. DOI: https://doi.org/10.3390/ijms20061350.</mixed-citation><mixed-citation xml:lang="en">Rohlwink UK, Walker NF, Ordonez AA, Li YJ, Tucker EW, Elkington PT, et al. Matrix metalloproteinases in pulmonary and central nervous system tuberculosis — a review. International Journal of Molecular Sciences. 2019;20(6):1350. DOI: https://doi.org/10.3390/ijms20061350.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Cao S, Li J, Lu J, Zhong R, Zhong H. Mycobacterium tuberculosis antigens repress Th1 immune response suppression and promotes lung cancer metastasis through PD-1/PDl-1 signaling pathway. Cell Death &amp; Disease. 2019;10(2):44. DOI: https://doi.org/10.1038/s41419-018-1237-y.</mixed-citation><mixed-citation xml:lang="en">Cao S, Li J, Lu J, Zhong R, Zhong H. Mycobacterium tuberculosis antigens repress Th1 immune response suppression and promotes lung cancer metastasis through PD-1/PDl-1 signaling pathway. Cell Death &amp; Disease. 2019;10(2):44. DOI: https://doi.org/10.1038/s41419-018-1237-y.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Voronina EV, Lobanova NV, Yakhin IR, Romanova NA, Seregin YA. Role of tumor necrosis factor alpha in immune pathogenesis of different diseases and its significance for evolving anticytokine therapy with monoclonal antibodies. Medical Immunology (Russia). 2018;20(6):797–806. (In Russ.) DOI: https://doi.org/10.15789/1563-0625-2018-6-797-806.</mixed-citation><mixed-citation xml:lang="en">Voronina EV, Lobanova NV, Yakhin IR, Romanova NA, Seregin YA. Role of tumor necrosis factor alpha in immune pathogenesis of different diseases and its significance for evolving anticytokine therapy with monoclonal antibodies. Medical Immunology (Russia). 2018;20(6):797–806. (In Russ.) DOI: https://doi.org/10.15789/1563-0625-2018-6-797-806.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Liu W, Chen X, He Y, Tian Y, Xu L, Ma Y, et al. TNF-α inhibits xenograft tumor formation by A549 lung cancer cells in nude mice via the HIF-1α/VASP signaling pathway. Oncology Reports. 2019;41(4):2418–2430. DOI: https://doi.org/10.3892/or.2019.7026.</mixed-citation><mixed-citation xml:lang="en">Liu W, Chen X, He Y, Tian Y, Xu L, Ma Y, et al. TNF-α inhibits xenograft tumor formation by A549 lung cancer cells in nude mice via the HIF-1α/VASP signaling pathway. Oncology Reports. 2019;41(4):2418–2430. DOI: https://doi.org/10.3892/or.2019.7026.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Benoot T, Piccioni E, De Ridder K, Goyvaerts C. TNFα and immune checkpoint inhibition: Friend or foe for lung cancer? International Journal of Molecular Sciences. 2021;22(16):8691. DOI: https://doi.org/10.3390/ijms22168691.</mixed-citation><mixed-citation xml:lang="en">Benoot T, Piccioni E, De Ridder K, Goyvaerts C. TNFα and immune checkpoint inhibition: Friend or foe for lung cancer? International Journal of Molecular Sciences. 2021;22(16):8691. DOI: https://doi.org/10.3390/ijms22168691.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Mootoo A, Stylianou E, Arias MA, Reljic R. TNF-α in tuberculosis: A cytokine with a split personality. Inflammation &amp; Allergy-Drug Targets. 2009;8(1):53–62. DOI: https://doi.org/10.2174/187152809787582543.</mixed-citation><mixed-citation xml:lang="en">Mootoo A, Stylianou E, Arias MA, Reljic R. TNF-α in tuberculosis: A cytokine with a split personality. Inflammation &amp; Allergy-Drug Targets. 2009;8(1):53–62. DOI: https://doi.org/10.2174/187152809787582543.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Yuk JM, Kim JK, Kim IS, Jo EK. TNF in human tuberculosis: A double-edged sword. Immune Network. 2024;24(1):e4. DOI: https://doi.org/10.4110/in.2024.24.e4.</mixed-citation><mixed-citation xml:lang="en">Yuk JM, Kim JK, Kim IS, Jo EK. TNF in human tuberculosis: A double-edged sword. Immune Network. 2024;24(1):e4. DOI: https://doi.org/10.4110/in.2024.24.e4.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Shang GS, Liu L, Qin YW. IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition. Oncology Letters. 2017;13(6):4657–4660. DOI: https://doi.org/10.3892/ol.2017.6048.</mixed-citation><mixed-citation xml:lang="en">Shang GS, Liu L, Qin YW. IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition. Oncology Letters. 2017;13(6):4657–4660. DOI: https://doi.org/10.3892/ol.2017.6048.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Strzalka W, Ziemienowicz A. Proliferating cell nuclear antigen (PCNA): A key factor in DNA replication and cell cycle regulation. Annals of Botany. 2011;107(7):1127–1140. DOI: https://doi.org/10.1093/aob/mcq243.</mixed-citation><mixed-citation xml:lang="en">Strzalka W, Ziemienowicz A. Proliferating cell nuclear antigen (PCNA): A key factor in DNA replication and cell cycle regulation. Annals of Botany. 2011;107(7):1127–1140. DOI: https://doi.org/10.1093/aob/mcq243.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Peng B, Ortega J, Gu L, Chang Z, Li GM. Phosphorylation of proliferating cell nuclear antigen promotes cancer progression by activating the ATM/Akt/GSK3β/Snail signaling pathway. Journal of Biological Chemistry. 2019;294(17):7037–7045. DOI: https://doi.org/10.1074/jbc.RA119.007897.</mixed-citation><mixed-citation xml:lang="en">Peng B, Ortega J, Gu L, Chang Z, Li GM. Phosphorylation of proliferating cell nuclear antigen promotes cancer progression by activating the ATM/Akt/GSK3β/Snail signaling pathway. Journal of Biological Chemistry. 2019;294(17):7037–7045. DOI: https://doi.org/10.1074/jbc.RA119.007897.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Wang L, Kong W, Liu B, Zhang X. Proliferating cell nuclear antigen promotes cell proliferation and tumorigenesis by up-regulating STAT3 in non-small cell lung cancer. Biomedicine and Pharmacotherapy. 2018;104:595–602. DOI: https://doi.org/10.1016/j.biopha.2018.05.071.</mixed-citation><mixed-citation xml:lang="en">Wang L, Kong W, Liu B, Zhang X. Proliferating cell nuclear antigen promotes cell proliferation and tumorigenesis by up-regulating STAT3 in non-small cell lung cancer. Biomedicine and Pharmacotherapy. 2018;104:595–602. DOI: https://doi.org/10.1016/j.biopha.2018.05.071.</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Wu C, Zhu X, Xia L, Wang L, Yu W, Guo Q, et al. High expression of long noncoding RNA PCNA-AS1 promotes non-small-cell lung cancer cell proliferation and oncogenic activity via upregulating CCND1. Journal of Cancer. 2020;11(7):1959–1967. DOI: https://doi.org/10.7150/jca.39087.</mixed-citation><mixed-citation xml:lang="en">Wu C, Zhu X, Xia L, Wang L, Yu W, Guo Q, et al. High expression of long noncoding RNA PCNA-AS1 promotes non-small-cell lung cancer cell proliferation and oncogenic activity via upregulating CCND1. Journal of Cancer. 2020;11(7):1959–1967. DOI: https://doi.org/10.7150/jca.39087.</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Ye X, Ling B, Xu H, Li G, Zhao X, Xu J, et al. Clinical significance of high expression of proliferating cell nuclear antigen in non-small cell lung cancer. Medicine. 2020;99(16):e19755. DOI: https://doi.org/10.1097/MD.0000000000019755.</mixed-citation><mixed-citation xml:lang="en">Ye X, Ling B, Xu H, Li G, Zhao X, Xu J, et al. Clinical significance of high expression of proliferating cell nuclear antigen in non-small cell lung cancer. Medicine. 2020;99(16):e19755. DOI: https://doi.org/10.1097/MD.0000000000019755.</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Chen X, Sun J, Wang Y. Expressions of CD44, PCNA and MRP1 in lung cancer tissues and their effects on proliferation and invasion abilities of lung cancer cell line 95D. Journal of BUON. 2021;26(1):72–78. PMID: https://pubmed.gov/33721434.</mixed-citation><mixed-citation xml:lang="en">Chen X, Sun J, Wang Y. Expressions of CD44, PCNA and MRP1 in lung cancer tissues and their effects on proliferation and invasion abilities of lung cancer cell line 95D. Journal of BUON. 2021;26(1):72–78. PMID: https://pubmed.gov/33721434.</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Fan J, Zhou X, Huang J, Wang X, Che G. Prognostic roles of PCNA expressions in non-small cell lung cancer: A meta-analysis. International Journal of Clinical and Experimental Medicine. 2016;9(3):5655–5665. Available from: https://clck.ru/3PuS8f (accessed: 19 June 2025).</mixed-citation><mixed-citation xml:lang="en">Fan J, Zhou X, Huang J, Wang X, Che G. Prognostic roles of PCNA expressions in non-small cell lung cancer: A meta-analysis. International Journal of Clinical and Experimental Medicine. 2016;9(3):5655–5665. Available from: https://clck.ru/3PuS8f (accessed: 19 June 2025).</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Chai Q, Lu Z, Liu Z, Zhong Y, Zhang F, Qiu C, et al. Lung gene expression signatures suggest pathogenic links and molecular markers for pulmonary tuberculosis, adenocarcinoma and sarcoidosis. Communications Biology. 2020;3(1):604. DOI: https://doi.org/10.1038/s42003-020-01318-0.</mixed-citation><mixed-citation xml:lang="en">Chai Q, Lu Z, Liu Z, Zhong Y, Zhang F, Qiu C, et al. Lung gene expression signatures suggest pathogenic links and molecular markers for pulmonary tuberculosis, adenocarcinoma and sarcoidosis. Communications Biology. 2020;3(1):604. DOI: https://doi.org/10.1038/s42003-020-01318-0.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
