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Mechanism of miR-222 and miR-126 regulation and its role in asbestos-induced malignancy

S. Gaetani, F. Monaco, F. Alessandrini, A. Tagliabracci, A. Sabbatini, M. Bracci, M. Valentino, J. Neuzil, M. Amati, L. Santarelli, M. Tomasetti,

. 2020 ; 121 (-) : 105700. [pub] 20200204

Language English Country Netherlands

Document type Journal Article, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc20028320

MiR-222 and miR-126 are associated with asbestos exposure and the ensuing malignancy, but the mechanism(s) of their regulation remain unclear. We evaluated the mechanism by which asbestos regulates miR-222 and miR-126 expression in the context of cancer etiology. An 'in vitro' model of carcinogen-induced cell transformation was used based on exposing bronchial epithelium BEAS-2B cells to three different carcinogens including asbestos. Involvement of the EGFR pathway and the role of epigenetics have been investigated in carcinogen-transformed cells and in malignant mesothelioma, a neoplastic disease associated with asbestos exposure. Increased expression of miR-222 and miR-126 were found in asbestos-transformed cells, but not in cells exposed to arsenic and chrome. Asbestos-mediated activation of the EGFR pathway and macrophages-induced inflammation resulted in miR-222 upregulation, which was reversed by EGFR inhibition. Conversely, asbestos-induced miR-126 expression was affected neither by EGFR modulation nor inflammation. Rather than methylation of the miR-126 host gene EGFL7, epigenetic mechanism involving DNMT1- and PARP1-mediated chromatin remodeling was found to upregulate of miR-126 in asbestos-exposed cells, while miR-126 was downregulated in malignant cells. Analysis of MM tissue supported the role of PARP1 in miR-126 regulation. Therefore, activation of the EGFR pathway and the PARP1-mediated epigenetic regulation both play a role in asbestos-induced miRNA expression, associated with in asbestos-induced carcinogenesis and tumor progression.

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$a MiR-222 and miR-126 are associated with asbestos exposure and the ensuing malignancy, but the mechanism(s) of their regulation remain unclear. We evaluated the mechanism by which asbestos regulates miR-222 and miR-126 expression in the context of cancer etiology. An 'in vitro' model of carcinogen-induced cell transformation was used based on exposing bronchial epithelium BEAS-2B cells to three different carcinogens including asbestos. Involvement of the EGFR pathway and the role of epigenetics have been investigated in carcinogen-transformed cells and in malignant mesothelioma, a neoplastic disease associated with asbestos exposure. Increased expression of miR-222 and miR-126 were found in asbestos-transformed cells, but not in cells exposed to arsenic and chrome. Asbestos-mediated activation of the EGFR pathway and macrophages-induced inflammation resulted in miR-222 upregulation, which was reversed by EGFR inhibition. Conversely, asbestos-induced miR-126 expression was affected neither by EGFR modulation nor inflammation. Rather than methylation of the miR-126 host gene EGFL7, epigenetic mechanism involving DNMT1- and PARP1-mediated chromatin remodeling was found to upregulate of miR-126 in asbestos-exposed cells, while miR-126 was downregulated in malignant cells. Analysis of MM tissue supported the role of PARP1 in miR-126 regulation. Therefore, activation of the EGFR pathway and the PARP1-mediated epigenetic regulation both play a role in asbestos-induced miRNA expression, associated with in asbestos-induced carcinogenesis and tumor progression.
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$a Monaco, Federica $u Department of Clinical and Molecular Sciences, Section of Experimental and Occupational Medicine, Polytechnic University of Marche, Via Tronto 10/A, 60020, Ancona, Italy.
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$a Alessandrini, Federica $u Department of Biomedical Sciences and Public Health, Section of Legal Medicine, Polytechnic University of Marche, Via Tronto 10/A, 60020, Ancona, Italy.
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$a Tagliabracci, Adriano $u Department of Biomedical Sciences and Public Health, Section of Legal Medicine, Polytechnic University of Marche, Via Tronto 10/A, 60020, Ancona, Italy.
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$a Sabbatini, Armando $u Division of Thoracic Surgery, United Hospitals, Ancona, 60126, Italy.
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$a Bracci, Massimo $u Department of Clinical and Molecular Sciences, Section of Experimental and Occupational Medicine, Polytechnic University of Marche, Via Tronto 10/A, 60020, Ancona, Italy.
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$a Valentino, Matteo $u Department of Clinical and Molecular Sciences, Section of Experimental and Occupational Medicine, Polytechnic University of Marche, Via Tronto 10/A, 60020, Ancona, Italy.
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$a Neuzil, Jiri $u Mitochondria, Apoptosis and Cancer Research Group, School of Medical Science, Griffith University, Southport, 4222, Qld, Australia; Molecular Therapy Group, Institute of Biotechnology, Czech Academy of Sciences, Prague-West, 252 50, Czech Republic.
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$a Amati, Monica $u Department of Clinical and Molecular Sciences, Section of Experimental and Occupational Medicine, Polytechnic University of Marche, Via Tronto 10/A, 60020, Ancona, Italy.
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$a Tomasetti, Marco $u Department of Clinical and Molecular Sciences, Section of Experimental and Occupational Medicine, Polytechnic University of Marche, Via Tronto 10/A, 60020, Ancona, Italy. Electronic address: m.tomasetti@staff.univpm.it.
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