DEAD-box helicase 27 plays a tumor-promoter role by regulating the stem cell-like activity of human colorectal cancer cells
Cancer stem cells (CSCs) are responsible for all important characteristics of tumors. DEAD-box helicase 27 (DDX27) is a member of the DEAD-box RNA helicase family, and there have been only a few studies on DDX27 function in cancer cells. This study is aimed at exploring whether DDX27 has any relatio...
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| Veröffentlicht in: | OncoTargets and therapy 2019-01, Vol.12, p.233-241 |
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| container_title | OncoTargets and therapy |
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| creator | Yang, Chunxing Li, Daojiang Bai, Yang Song, Shenglei Yan, Peicheng Wu, Runliu Zhang, Yi Hu, Gui Lin, Changwei Li, Xiaorong Huang, Lihuang |
| description | Cancer stem cells (CSCs) are responsible for all important characteristics of tumors. DEAD-box helicase 27 (DDX27) is a member of the DEAD-box RNA helicase family, and there have been only a few studies on DDX27 function in cancer cells. This study is aimed at exploring whether DDX27 has any relation to tumorigenesis of colorectal cancer (CRC) and elucidating the potential mechanism.
Data from Catalog Of Somatic Mutations In Cancer, Gene Expression Omnibus, and The Cancer Genome Atlas databases reveal that DDX27 is overexpressed in CRC tissues. qRT-PCR and Western blots were used to evaluate the expression level of DDX27 in 40 paired clinical CRC samples. DDX27 was knockdown in HT29 and HCT116 cell line with shRNA. Then CCK-8, colony formation assay and flow cytometry assay were performed to examine proliferative ability, cell cycle and sensitivity to 5-fluorouracil. Sphere-formation assay and in vivo subcutaneous tumor-formation assay were used to assess self-renewal in vitro and vivo as well as the tumor-initiating potential.
DDX27 is upregulated in CRC tissues and downregulation of DDX27 inhibits proliferation of colorectal cancer cell and promotes sensitivity to 5-fluorouracil. Downregulation of DDX27 can downregulate the gene expression of known CSC markers in CRC cells, inhibit sphere-formation ability, and promote colonosphere differentiation. Downregulation of DDX27 in CSCs can decrease the tumor-initiating ability of CRC cells in vivo.
DDX27 may play a tumorpromoter role of CRC by regulating the stem cell-like activity of CRC cells. |
| doi_str_mv | 10.2147/OTT.S190814 |
| format | Article |
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Data from Catalog Of Somatic Mutations In Cancer, Gene Expression Omnibus, and The Cancer Genome Atlas databases reveal that DDX27 is overexpressed in CRC tissues. qRT-PCR and Western blots were used to evaluate the expression level of DDX27 in 40 paired clinical CRC samples. DDX27 was knockdown in HT29 and HCT116 cell line with shRNA. Then CCK-8, colony formation assay and flow cytometry assay were performed to examine proliferative ability, cell cycle and sensitivity to 5-fluorouracil. Sphere-formation assay and in vivo subcutaneous tumor-formation assay were used to assess self-renewal in vitro and vivo as well as the tumor-initiating potential.
DDX27 is upregulated in CRC tissues and downregulation of DDX27 inhibits proliferation of colorectal cancer cell and promotes sensitivity to 5-fluorouracil. Downregulation of DDX27 can downregulate the gene expression of known CSC markers in CRC cells, inhibit sphere-formation ability, and promote colonosphere differentiation. Downregulation of DDX27 in CSCs can decrease the tumor-initiating ability of CRC cells in vivo.
DDX27 may play a tumorpromoter role of CRC by regulating the stem cell-like activity of CRC cells.</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><identifier>DOI: 10.2147/OTT.S190814</identifier><identifier>PMID: 30643421</identifier><language>eng</language><publisher>New Zealand: Dove Medical Press Limited</publisher><subject>5-Fluorouracil ; Breast cancer ; Cancer ; Cancer cells ; Cancer therapies ; Cell cycle ; Cell self-renewal ; Chemotherapy ; Colorectal cancer ; Fluorouracil ; Gastric cancer ; Gene expression ; Genetic aspects ; Genomes ; Genomics ; Laboratories ; Leukemia ; Medical prognosis ; Metastasis ; Original Research ; Proteins ; RNA ; Stem cells ; Tumors</subject><ispartof>OncoTargets and therapy, 2019-01, Vol.12, p.233-241</ispartof><rights>COPYRIGHT 2019 Dove Medical Press Limited</rights><rights>2019. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 Yang et al. This work is published and licensed by Dove Medical Press Limited 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c615t-c44fd2fbd4eca43a829780fbfb78733a110f3d2702e44fbe6cd5760a0621eba13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6314319/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6314319/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,3849,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30643421$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Chunxing</creatorcontrib><creatorcontrib>Li, Daojiang</creatorcontrib><creatorcontrib>Bai, Yang</creatorcontrib><creatorcontrib>Song, Shenglei</creatorcontrib><creatorcontrib>Yan, Peicheng</creatorcontrib><creatorcontrib>Wu, Runliu</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><creatorcontrib>Hu, Gui</creatorcontrib><creatorcontrib>Lin, Changwei</creatorcontrib><creatorcontrib>Li, Xiaorong</creatorcontrib><creatorcontrib>Huang, Lihuang</creatorcontrib><title>DEAD-box helicase 27 plays a tumor-promoter role by regulating the stem cell-like activity of human colorectal cancer cells</title><title>OncoTargets and therapy</title><addtitle>Onco Targets Ther</addtitle><description>Cancer stem cells (CSCs) are responsible for all important characteristics of tumors. DEAD-box helicase 27 (DDX27) is a member of the DEAD-box RNA helicase family, and there have been only a few studies on DDX27 function in cancer cells. This study is aimed at exploring whether DDX27 has any relation to tumorigenesis of colorectal cancer (CRC) and elucidating the potential mechanism.
Data from Catalog Of Somatic Mutations In Cancer, Gene Expression Omnibus, and The Cancer Genome Atlas databases reveal that DDX27 is overexpressed in CRC tissues. qRT-PCR and Western blots were used to evaluate the expression level of DDX27 in 40 paired clinical CRC samples. DDX27 was knockdown in HT29 and HCT116 cell line with shRNA. Then CCK-8, colony formation assay and flow cytometry assay were performed to examine proliferative ability, cell cycle and sensitivity to 5-fluorouracil. Sphere-formation assay and in vivo subcutaneous tumor-formation assay were used to assess self-renewal in vitro and vivo as well as the tumor-initiating potential.
DDX27 is upregulated in CRC tissues and downregulation of DDX27 inhibits proliferation of colorectal cancer cell and promotes sensitivity to 5-fluorouracil. Downregulation of DDX27 can downregulate the gene expression of known CSC markers in CRC cells, inhibit sphere-formation ability, and promote colonosphere differentiation. Downregulation of DDX27 in CSCs can decrease the tumor-initiating ability of CRC cells in vivo.
DDX27 may play a tumorpromoter role of CRC by regulating the stem cell-like activity of CRC cells.</description><subject>5-Fluorouracil</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell self-renewal</subject><subject>Chemotherapy</subject><subject>Colorectal cancer</subject><subject>Fluorouracil</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Laboratories</subject><subject>Leukemia</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Original Research</subject><subject>Proteins</subject><subject>RNA</subject><subject>Stem cells</subject><subject>Tumors</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptks9rFDEUxwdRbK2evEtAEKHMml-TzFyEpa1VKPTgeg6ZzJud1MxkTTLFxX_eLF3rrkgOCcnnfcJ7fIviNcELSrj8cLtaLb6SBteEPylOCZF1KRqGnx6cT4oXMd5hLERN-fPihGHBGafktPh1ebW8LFv_Ew3grNEREJVo4_Q2Io3SPPpQboIffYKAgneA2i0KsJ6dTnZaozQAiglGZMC50tnvgLRJ9t6mLfI9GuZRT8h45wOYpB0yejLZtKPjy-JZr12EV_v9rPj26Wp18bm8ub3-crG8KY0gVSoN531H-7bjYDRnuqaNrHHf9q2sJWOaENyzjkpMIZMtCNNVUmCNBSXQasLOio8P3s3cjtAZmFLQTm2CHXXYKq-tOn6Z7KDW_l4JRjgjTRa83wuC_zFDTGq0cdeCnsDPUVEiG1YRWtGMvv0HvfNzmHJ7ilJOBeeY1n-ptXag7NT7_K_ZSdVS1JJwzCuRqcV_qLw6GK3xE_Q23x8VvDsoGEC7NETv5mT9FI_B8wfQBB9jgP5xGASrXahUDpXahyrTbw7n98j-SRH7DY4bxn4</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Yang, Chunxing</creator><creator>Li, Daojiang</creator><creator>Bai, Yang</creator><creator>Song, Shenglei</creator><creator>Yan, Peicheng</creator><creator>Wu, Runliu</creator><creator>Zhang, Yi</creator><creator>Hu, Gui</creator><creator>Lin, Changwei</creator><creator>Li, Xiaorong</creator><creator>Huang, Lihuang</creator><general>Dove Medical Press Limited</general><general>Taylor & Francis Ltd</general><general>Dove Medical Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</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>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190101</creationdate><title>DEAD-box helicase 27 plays a tumor-promoter role by regulating the stem cell-like activity of human colorectal cancer cells</title><author>Yang, Chunxing ; Li, Daojiang ; Bai, Yang ; Song, Shenglei ; Yan, Peicheng ; Wu, Runliu ; Zhang, Yi ; Hu, Gui ; Lin, Changwei ; Li, Xiaorong ; Huang, Lihuang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c615t-c44fd2fbd4eca43a829780fbfb78733a110f3d2702e44fbe6cd5760a0621eba13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>5-Fluorouracil</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell self-renewal</topic><topic>Chemotherapy</topic><topic>Colorectal cancer</topic><topic>Fluorouracil</topic><topic>Gastric cancer</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Laboratories</topic><topic>Leukemia</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Original Research</topic><topic>Proteins</topic><topic>RNA</topic><topic>Stem cells</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Chunxing</creatorcontrib><creatorcontrib>Li, Daojiang</creatorcontrib><creatorcontrib>Bai, Yang</creatorcontrib><creatorcontrib>Song, Shenglei</creatorcontrib><creatorcontrib>Yan, Peicheng</creatorcontrib><creatorcontrib>Wu, Runliu</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><creatorcontrib>Hu, Gui</creatorcontrib><creatorcontrib>Lin, Changwei</creatorcontrib><creatorcontrib>Li, Xiaorong</creatorcontrib><creatorcontrib>Huang, Lihuang</creatorcontrib><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>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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</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>Research Library Prep</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>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>OncoTargets and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Chunxing</au><au>Li, Daojiang</au><au>Bai, Yang</au><au>Song, Shenglei</au><au>Yan, Peicheng</au><au>Wu, Runliu</au><au>Zhang, Yi</au><au>Hu, Gui</au><au>Lin, Changwei</au><au>Li, Xiaorong</au><au>Huang, Lihuang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DEAD-box helicase 27 plays a tumor-promoter role by regulating the stem cell-like activity of human colorectal cancer cells</atitle><jtitle>OncoTargets and therapy</jtitle><addtitle>Onco Targets Ther</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>12</volume><spage>233</spage><epage>241</epage><pages>233-241</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>Cancer stem cells (CSCs) are responsible for all important characteristics of tumors. DEAD-box helicase 27 (DDX27) is a member of the DEAD-box RNA helicase family, and there have been only a few studies on DDX27 function in cancer cells. This study is aimed at exploring whether DDX27 has any relation to tumorigenesis of colorectal cancer (CRC) and elucidating the potential mechanism.
Data from Catalog Of Somatic Mutations In Cancer, Gene Expression Omnibus, and The Cancer Genome Atlas databases reveal that DDX27 is overexpressed in CRC tissues. qRT-PCR and Western blots were used to evaluate the expression level of DDX27 in 40 paired clinical CRC samples. DDX27 was knockdown in HT29 and HCT116 cell line with shRNA. Then CCK-8, colony formation assay and flow cytometry assay were performed to examine proliferative ability, cell cycle and sensitivity to 5-fluorouracil. Sphere-formation assay and in vivo subcutaneous tumor-formation assay were used to assess self-renewal in vitro and vivo as well as the tumor-initiating potential.
DDX27 is upregulated in CRC tissues and downregulation of DDX27 inhibits proliferation of colorectal cancer cell and promotes sensitivity to 5-fluorouracil. Downregulation of DDX27 can downregulate the gene expression of known CSC markers in CRC cells, inhibit sphere-formation ability, and promote colonosphere differentiation. Downregulation of DDX27 in CSCs can decrease the tumor-initiating ability of CRC cells in vivo.
DDX27 may play a tumorpromoter role of CRC by regulating the stem cell-like activity of CRC cells.</abstract><cop>New Zealand</cop><pub>Dove Medical Press Limited</pub><pmid>30643421</pmid><doi>10.2147/OTT.S190814</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Taylor & Francis Open Access; DOVE Medical Press Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | 5-Fluorouracil Breast cancer Cancer Cancer cells Cancer therapies Cell cycle Cell self-renewal Chemotherapy Colorectal cancer Fluorouracil Gastric cancer Gene expression Genetic aspects Genomes Genomics Laboratories Leukemia Medical prognosis Metastasis Original Research Proteins RNA Stem cells Tumors |
| title | DEAD-box helicase 27 plays a tumor-promoter role by regulating the stem cell-like activity of human colorectal cancer cells |
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