Effects of diesel exhaust particles on microRNA-21 in human bronchial epithelial cells and potential carcinogenic mechanisms
Air pollution plays a role in cancer risk, particularly in lung cancer, which is the leading cause of cancer-related mortality worldwide. Diesel exhaust particles (DEPs), a component of diesel exhaust products, is a complex mixture of particle compounds that include a large number of known and suspe...
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Veröffentlicht in: | Molecular medicine reports 2015-08, Vol.12 (2), p.2329-2335 |
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description | Air pollution plays a role in cancer risk, particularly in lung cancer, which is the leading cause of cancer-related mortality worldwide. Diesel exhaust particles (DEPs), a component of diesel exhaust products, is a complex mixture of particle compounds that include a large number of known and suspected human carcinogens. Historically, lung cancer, which is associated with DEPs, has been the focus of attention as a health risk in human and animal studies. However, the mechanism by which DEPs cause lung cancer remains unclear. The present study reports that DEPs increased miR-21 expression and then activated the PTEN/PI3K/AKT pathway in human bronchial epithelial (HBE) cells, which may serve as an important carcinogenic mechanism. However, the data revealed that short-term exposure to a high DEP concentration did not cause evident cell carcinogenesis in HBE cells. |
doi_str_mv | 10.3892/mmr.2015.3655 |
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Diesel exhaust particles (DEPs), a component of diesel exhaust products, is a complex mixture of particle compounds that include a large number of known and suspected human carcinogens. Historically, lung cancer, which is associated with DEPs, has been the focus of attention as a health risk in human and animal studies. However, the mechanism by which DEPs cause lung cancer remains unclear. The present study reports that DEPs increased miR-21 expression and then activated the PTEN/PI3K/AKT pathway in human bronchial epithelial (HBE) cells, which may serve as an important carcinogenic mechanism. However, the data revealed that short-term exposure to a high DEP concentration did not cause evident cell carcinogenesis in HBE cells.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2015.3655</identifier><identifier>PMID: 25901472</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>1-Phosphatidylinositol 3-kinase ; Air pollution ; AKT protein ; antisense oligonucleotide of microRNA-21 ; Apoptosis ; Apoptosis - drug effects ; Bronchi - drug effects ; Bronchi - metabolism ; Bronchi - pathology ; Cancer therapies ; Carcinogenesis ; Carcinogens ; Carcinogens - toxicity ; Cell cycle ; Cell Cycle - drug effects ; Cell Line ; Cell Line, Tumor ; Cell Movement - drug effects ; Collagen - chemistry ; Development and progression ; Diesel ; diesel exhaust particles ; Diesel fuels ; Diesel motor exhaust gas ; Drug Combinations ; Epithelial cells ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Fluorides ; Gene expression ; Gene Expression Regulation ; Genetic aspects ; Health aspects ; Humans ; Kinases ; Laboratories ; Laminin - chemistry ; lung adenocarcinoma cells ; Lung cancer ; Lung diseases ; MicroRNA ; microRNA-21 ; MicroRNAs ; MicroRNAs - agonists ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Morphology ; normal human bronchial epithelial cells ; Outdoor air quality ; Particles ; Particulate Matter - toxicity ; Penicillin ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Properties ; Proteins ; Proteoglycans - chemistry ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; PTEN protein ; Signal transduction ; Signal Transduction - drug effects ; Studies ; Tumorigenesis ; Vehicle Emissions - toxicity</subject><ispartof>Molecular medicine reports, 2015-08, Vol.12 (2), p.2329-2335</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-10f9a40b568232e93cacf563770a7e9f83107a52a44954231d7712b0e26604b63</citedby><cites>FETCH-LOGICAL-c459t-10f9a40b568232e93cacf563770a7e9f83107a52a44954231d7712b0e26604b63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25901472$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHOU, FANG</creatorcontrib><creatorcontrib>LI, SULI</creatorcontrib><creatorcontrib>JIA, WENLIANG</creatorcontrib><creatorcontrib>LV, GANG</creatorcontrib><creatorcontrib>SONG, CHONGLIN</creatorcontrib><creatorcontrib>KANG, CHUNSHENG</creatorcontrib><creatorcontrib>ZHANG, QINGYU</creatorcontrib><title>Effects of diesel exhaust particles on microRNA-21 in human bronchial epithelial cells and potential carcinogenic mechanisms</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Air pollution plays a role in cancer risk, particularly in lung cancer, which is the leading cause of cancer-related mortality worldwide. Diesel exhaust particles (DEPs), a component of diesel exhaust products, is a complex mixture of particle compounds that include a large number of known and suspected human carcinogens. Historically, lung cancer, which is associated with DEPs, has been the focus of attention as a health risk in human and animal studies. However, the mechanism by which DEPs cause lung cancer remains unclear. The present study reports that DEPs increased miR-21 expression and then activated the PTEN/PI3K/AKT pathway in human bronchial epithelial (HBE) cells, which may serve as an important carcinogenic mechanism. However, the data revealed that short-term exposure to a high DEP concentration did not cause evident cell carcinogenesis in HBE cells.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Air pollution</subject><subject>AKT protein</subject><subject>antisense oligonucleotide of microRNA-21</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bronchi - drug effects</subject><subject>Bronchi - metabolism</subject><subject>Bronchi - pathology</subject><subject>Cancer therapies</subject><subject>Carcinogenesis</subject><subject>Carcinogens</subject><subject>Carcinogens - toxicity</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Collagen - chemistry</subject><subject>Development and progression</subject><subject>Diesel</subject><subject>diesel exhaust particles</subject><subject>Diesel fuels</subject><subject>Diesel motor exhaust gas</subject><subject>Drug Combinations</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Fluorides</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Laminin - chemistry</subject><subject>lung adenocarcinoma cells</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>MicroRNA</subject><subject>microRNA-21</subject><subject>MicroRNAs</subject><subject>MicroRNAs - agonists</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Morphology</subject><subject>normal human bronchial epithelial cells</subject><subject>Outdoor air quality</subject><subject>Particles</subject><subject>Particulate Matter - toxicity</subject><subject>Penicillin</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Properties</subject><subject>Proteins</subject><subject>Proteoglycans - chemistry</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>PTEN protein</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Studies</subject><subject>Tumorigenesis</subject><subject>Vehicle Emissions - toxicity</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc1rFTEUxQex2FpdupWAC1d55nPysnyUaoWiUNp1yGRuOikzyZjMQAX_ePP6nkVBAsnl5nduwjlN846SDd9q9mma8oYRKje8lfJFc0aVppgTIl4ea6a1Om1el_JASCuZ1K-a07oTKhQ7a35deg9uKSh51AcoMCJ4HOxaFjTbvAQ3Qr2LaAoup5tvO8woChEN62Qj6nKKbgi2auawDDDuSwfjWJCNPZrTAnF56tnsQkz3EINDE7jBxlCm8qY58XYs8PZ4njd3ny9vL67w9fcvXy9219gJqRdMiddWkE62W8YZaO6s87LlShGrQPstp0RZyawQWgrGaa8UZR0B1rZEdC0_bz4c5s45_VihLOYhrTnWJw3VnAlFt-Iv6t6OYEL0acnWTaE4sxNMtqoaRiu1-Q9VVw_VoxTBh9r_R4APgmpgKRm8mXOYbP5pKDH7CE2N0OwjNPsIK__--Nm1m6B_pv9kVoGPB6DM1eXQp_LM1EmYMkwYrkZp_hsKH6Js</recordid><startdate>20150801</startdate><enddate>20150801</enddate><creator>ZHOU, FANG</creator><creator>LI, SULI</creator><creator>JIA, WENLIANG</creator><creator>LV, GANG</creator><creator>SONG, CHONGLIN</creator><creator>KANG, CHUNSHENG</creator><creator>ZHANG, QINGYU</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20150801</creationdate><title>Effects of diesel exhaust particles on microRNA-21 in human bronchial epithelial cells and potential carcinogenic mechanisms</title><author>ZHOU, FANG ; LI, SULI ; JIA, WENLIANG ; LV, GANG ; SONG, CHONGLIN ; KANG, CHUNSHENG ; ZHANG, QINGYU</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-10f9a40b568232e93cacf563770a7e9f83107a52a44954231d7712b0e26604b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Air pollution</topic><topic>AKT protein</topic><topic>antisense oligonucleotide of microRNA-21</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Bronchi - drug effects</topic><topic>Bronchi - metabolism</topic><topic>Bronchi - pathology</topic><topic>Cancer therapies</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Carcinogens - toxicity</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Collagen - chemistry</topic><topic>Development and progression</topic><topic>Diesel</topic><topic>diesel exhaust particles</topic><topic>Diesel fuels</topic><topic>Diesel motor exhaust gas</topic><topic>Drug Combinations</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Fluorides</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Laminin - chemistry</topic><topic>lung adenocarcinoma cells</topic><topic>Lung cancer</topic><topic>Lung diseases</topic><topic>MicroRNA</topic><topic>microRNA-21</topic><topic>MicroRNAs</topic><topic>MicroRNAs - agonists</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Morphology</topic><topic>normal human bronchial epithelial cells</topic><topic>Outdoor air quality</topic><topic>Particles</topic><topic>Particulate Matter - toxicity</topic><topic>Penicillin</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Properties</topic><topic>Proteins</topic><topic>Proteoglycans - chemistry</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>PTEN protein</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Studies</topic><topic>Tumorigenesis</topic><topic>Vehicle Emissions - toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHOU, FANG</creatorcontrib><creatorcontrib>LI, SULI</creatorcontrib><creatorcontrib>JIA, WENLIANG</creatorcontrib><creatorcontrib>LV, GANG</creatorcontrib><creatorcontrib>SONG, CHONGLIN</creatorcontrib><creatorcontrib>KANG, CHUNSHENG</creatorcontrib><creatorcontrib>ZHANG, QINGYU</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHOU, FANG</au><au>LI, SULI</au><au>JIA, WENLIANG</au><au>LV, GANG</au><au>SONG, CHONGLIN</au><au>KANG, CHUNSHENG</au><au>ZHANG, QINGYU</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of diesel exhaust particles on microRNA-21 in human bronchial epithelial cells and potential carcinogenic mechanisms</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2015-08-01</date><risdate>2015</risdate><volume>12</volume><issue>2</issue><spage>2329</spage><epage>2335</epage><pages>2329-2335</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Air pollution plays a role in cancer risk, particularly in lung cancer, which is the leading cause of cancer-related mortality worldwide. Diesel exhaust particles (DEPs), a component of diesel exhaust products, is a complex mixture of particle compounds that include a large number of known and suspected human carcinogens. Historically, lung cancer, which is associated with DEPs, has been the focus of attention as a health risk in human and animal studies. However, the mechanism by which DEPs cause lung cancer remains unclear. The present study reports that DEPs increased miR-21 expression and then activated the PTEN/PI3K/AKT pathway in human bronchial epithelial (HBE) cells, which may serve as an important carcinogenic mechanism. However, the data revealed that short-term exposure to a high DEP concentration did not cause evident cell carcinogenesis in HBE cells.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25901472</pmid><doi>10.3892/mmr.2015.3655</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase Air pollution AKT protein antisense oligonucleotide of microRNA-21 Apoptosis Apoptosis - drug effects Bronchi - drug effects Bronchi - metabolism Bronchi - pathology Cancer therapies Carcinogenesis Carcinogens Carcinogens - toxicity Cell cycle Cell Cycle - drug effects Cell Line Cell Line, Tumor Cell Movement - drug effects Collagen - chemistry Development and progression Diesel diesel exhaust particles Diesel fuels Diesel motor exhaust gas Drug Combinations Epithelial cells Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - pathology Fluorides Gene expression Gene Expression Regulation Genetic aspects Health aspects Humans Kinases Laboratories Laminin - chemistry lung adenocarcinoma cells Lung cancer Lung diseases MicroRNA microRNA-21 MicroRNAs MicroRNAs - agonists MicroRNAs - genetics MicroRNAs - metabolism miRNA Morphology normal human bronchial epithelial cells Outdoor air quality Particles Particulate Matter - toxicity Penicillin Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Properties Proteins Proteoglycans - chemistry Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism PTEN protein Signal transduction Signal Transduction - drug effects Studies Tumorigenesis Vehicle Emissions - toxicity |
title | Effects of diesel exhaust particles on microRNA-21 in human bronchial epithelial cells and potential carcinogenic mechanisms |
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