Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells
Objectives: Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential tar...
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| Veröffentlicht in: | Technology in cancer research & treatment 2019, Vol.18, p.1533033819842546-1533033819842546 |
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| container_title | Technology in cancer research & treatment |
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| creator | Ao, Nannan Dai, Yingchu Chen, Qianping Feng, Yang Yu, Jingping Wang, Chang Liu, Fenju Li, Ming Liu, Geng |
| description | Objectives:
Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways.
Methods:
Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction.
Results:
The proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G2/M arrest and apoptosis. Microarray chips revealed multiple signaling pathways targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt-, and calcium-mediated pathway. The expression patterns of 4 representative genes UBD, CUL3, HDAC6, and GADD45A were verified by quantitative real-time polymerase chain reaction and showed consistency with the microarray assay.
Conclusion:
Bortezomib could suppress cell viability, cause G2/M arrest, and induce apoptosis in human esophageal cancer cells, with possible targets including UBD, CUL3, HDAC6, and GADD45A. |
| doi_str_mv | 10.1177/1533033819842546 |
| format | Article |
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Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways.
Methods:
Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction.
Results:
The proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G2/M arrest and apoptosis. Microarray chips revealed multiple signaling pathways targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt-, and calcium-mediated pathway. The expression patterns of 4 representative genes UBD, CUL3, HDAC6, and GADD45A were verified by quantitative real-time polymerase chain reaction and showed consistency with the microarray assay.
Conclusion:
Bortezomib could suppress cell viability, cause G2/M arrest, and induce apoptosis in human esophageal cancer cells, with possible targets including UBD, CUL3, HDAC6, and GADD45A.</description><identifier>ISSN: 1533-0346</identifier><identifier>EISSN: 1533-0338</identifier><identifier>DOI: 10.1177/1533033819842546</identifier><identifier>PMID: 30961474</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Annexin V ; Apoptosis ; Apoptosis - drug effects ; Bortezomib ; Bortezomib - pharmacology ; Calcium (reticular) ; Carcinoma - drug therapy ; Carcinoma - genetics ; Carcinoma - pathology ; Cell cycle ; Cell Cycle Proteins - genetics ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cell viability ; Cullin Proteins - genetics ; DNA microarrays ; Endoplasmic reticulum ; Epithelial cells ; Epithelial Cells - drug effects ; Esophageal cancer ; Esophageal carcinoma ; Esophageal Neoplasms - drug therapy ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; Esophagus ; Flow Cytometry ; G2 Phase Cell Cycle Checkpoints - drug effects ; Gadd45A protein ; Gene Expression Regulation, Neoplastic - drug effects ; Genomes ; Histone Deacetylase 6 - genetics ; Humans ; Microarray Analysis ; mRNA ; Multiple myeloma ; Neoplasm Proteins - genetics ; Original ; Polymerase chain reaction ; Propidium iodide ; Proteasomes ; RNA, Messenger - genetics ; Solid tumors ; Targeted cancer therapy ; Tumor cell lines ; Ubiquitins - genetics ; Wnt protein ; Wnt Signaling Pathway - drug effects</subject><ispartof>Technology in cancer research & treatment, 2019, Vol.18, p.1533033819842546-1533033819842546</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. This work is licensed under the Creative Commons Attribution – Non-Commercial License http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2019 2019 SAGE Publications</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-70e2f1d51514565a3da3946cdd3c6d6dbb193508c68c22d37c1eaf844e9f842b3</citedby><cites>FETCH-LOGICAL-c462t-70e2f1d51514565a3da3946cdd3c6d6dbb193508c68c22d37c1eaf844e9f842b3</cites><orcidid>0000-0001-6245-7653</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6457034/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6457034/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,4024,21966,27853,27923,27924,27925,44945,45333,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30961474$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ao, Nannan</creatorcontrib><creatorcontrib>Dai, Yingchu</creatorcontrib><creatorcontrib>Chen, Qianping</creatorcontrib><creatorcontrib>Feng, Yang</creatorcontrib><creatorcontrib>Yu, Jingping</creatorcontrib><creatorcontrib>Wang, Chang</creatorcontrib><creatorcontrib>Liu, Fenju</creatorcontrib><creatorcontrib>Li, Ming</creatorcontrib><creatorcontrib>Liu, Geng</creatorcontrib><title>Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells</title><title>Technology in cancer research & treatment</title><addtitle>Technol Cancer Res Treat</addtitle><description>Objectives:
Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways.
Methods:
Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction.
Results:
The proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G2/M arrest and apoptosis. Microarray chips revealed multiple signaling pathways targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt-, and calcium-mediated pathway. The expression patterns of 4 representative genes UBD, CUL3, HDAC6, and GADD45A were verified by quantitative real-time polymerase chain reaction and showed consistency with the microarray assay.
Conclusion:
Bortezomib could suppress cell viability, cause G2/M arrest, and induce apoptosis in human esophageal cancer cells, with possible targets including UBD, CUL3, HDAC6, and GADD45A.</description><subject>Annexin V</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bortezomib</subject><subject>Bortezomib - pharmacology</subject><subject>Calcium (reticular)</subject><subject>Carcinoma - drug therapy</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - pathology</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Cullin Proteins - genetics</subject><subject>DNA microarrays</subject><subject>Endoplasmic reticulum</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - drug effects</subject><subject>Esophageal cancer</subject><subject>Esophageal carcinoma</subject><subject>Esophageal Neoplasms - drug therapy</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophagus</subject><subject>Flow Cytometry</subject><subject>G2 Phase Cell Cycle Checkpoints - drug effects</subject><subject>Gadd45A protein</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genomes</subject><subject>Histone Deacetylase 6 - genetics</subject><subject>Humans</subject><subject>Microarray Analysis</subject><subject>mRNA</subject><subject>Multiple myeloma</subject><subject>Neoplasm Proteins - genetics</subject><subject>Original</subject><subject>Polymerase chain reaction</subject><subject>Propidium iodide</subject><subject>Proteasomes</subject><subject>RNA, Messenger - genetics</subject><subject>Solid tumors</subject><subject>Targeted cancer therapy</subject><subject>Tumor cell lines</subject><subject>Ubiquitins - genetics</subject><subject>Wnt protein</subject><subject>Wnt Signaling Pathway - drug effects</subject><issn>1533-0346</issn><issn>1533-0338</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1UU1v1DAUtBCIloU7J2SJSy-h_k5yQaKrpUWqBIcijpZjP--6SuLFThDl1-Noy0Ir4YP9NJ4Ze95D6DUl7yit63MqOSecN7RtBJNCPUGnC1Qt2NNjLdQJepHzLSFMKU6foxNOWkVFLU6Rv4QxDlB9Cw7wlxR96MO4xdHjaQf4Jv4MFm-8Bzst2EVME_yKQ-hwHPHVPJgRb3Lc78wWTI_XJtlQ7Aze7EPR92EBoe_zS_TMmz7Dq_tzhb5-3Nysr6rrz5ef1h-uKysUm6qaAPPUSSqpkEoa7gxvhbLOcauccl1HWy5JY1VjGXO8thSMb4SAtuys4yv0_uC7n7sBnIVxSqbX-xQGk-50NEE_vBnDTm_jD62ErEunisHZvUGK32fIkx5CtiWCGSHOWTNGFFtaXRfq20fU2zinscTTjFMmGeVlrRA5sGyKOSfwx89Qopch6sdDLJI3_4Y4Cv5MrRCqAyGXvv999b-GvwE3gKP8</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Ao, Nannan</creator><creator>Dai, Yingchu</creator><creator>Chen, Qianping</creator><creator>Feng, Yang</creator><creator>Yu, Jingping</creator><creator>Wang, Chang</creator><creator>Liu, Fenju</creator><creator>Li, Ming</creator><creator>Liu, Geng</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>AFRWT</scope><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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6245-7653</orcidid></search><sort><creationdate>2019</creationdate><title>Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells</title><author>Ao, Nannan ; Dai, Yingchu ; Chen, Qianping ; Feng, Yang ; Yu, Jingping ; Wang, Chang ; Liu, Fenju ; Li, Ming ; Liu, Geng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-70e2f1d51514565a3da3946cdd3c6d6dbb193508c68c22d37c1eaf844e9f842b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Annexin V</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Bortezomib</topic><topic>Bortezomib - pharmacology</topic><topic>Calcium (reticular)</topic><topic>Carcinoma - drug therapy</topic><topic>Carcinoma - genetics</topic><topic>Carcinoma - pathology</topic><topic>Cell cycle</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Cullin Proteins - genetics</topic><topic>DNA microarrays</topic><topic>Endoplasmic reticulum</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - drug effects</topic><topic>Esophageal cancer</topic><topic>Esophageal carcinoma</topic><topic>Esophageal Neoplasms - drug therapy</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophagus</topic><topic>Flow Cytometry</topic><topic>G2 Phase Cell Cycle Checkpoints - drug effects</topic><topic>Gadd45A protein</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genomes</topic><topic>Histone Deacetylase 6 - genetics</topic><topic>Humans</topic><topic>Microarray Analysis</topic><topic>mRNA</topic><topic>Multiple myeloma</topic><topic>Neoplasm Proteins - genetics</topic><topic>Original</topic><topic>Polymerase chain reaction</topic><topic>Propidium iodide</topic><topic>Proteasomes</topic><topic>RNA, Messenger - genetics</topic><topic>Solid tumors</topic><topic>Targeted cancer therapy</topic><topic>Tumor cell lines</topic><topic>Ubiquitins - genetics</topic><topic>Wnt protein</topic><topic>Wnt Signaling Pathway - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ao, Nannan</creatorcontrib><creatorcontrib>Dai, Yingchu</creatorcontrib><creatorcontrib>Chen, Qianping</creatorcontrib><creatorcontrib>Feng, Yang</creatorcontrib><creatorcontrib>Yu, Jingping</creatorcontrib><creatorcontrib>Wang, Chang</creatorcontrib><creatorcontrib>Liu, Fenju</creatorcontrib><creatorcontrib>Li, Ming</creatorcontrib><creatorcontrib>Liu, Geng</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</collection><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>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>ProQuest Central Essentials</collection><collection>ProQuest Central</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Technology in cancer research & treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ao, Nannan</au><au>Dai, Yingchu</au><au>Chen, Qianping</au><au>Feng, Yang</au><au>Yu, Jingping</au><au>Wang, Chang</au><au>Liu, Fenju</au><au>Li, Ming</au><au>Liu, Geng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells</atitle><jtitle>Technology in cancer research & treatment</jtitle><addtitle>Technol Cancer Res Treat</addtitle><date>2019</date><risdate>2019</risdate><volume>18</volume><spage>1533033819842546</spage><epage>1533033819842546</epage><pages>1533033819842546-1533033819842546</pages><issn>1533-0346</issn><eissn>1533-0338</eissn><abstract>Objectives:
Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways.
Methods:
Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction.
Results:
The proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G2/M arrest and apoptosis. Microarray chips revealed multiple signaling pathways targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt-, and calcium-mediated pathway. The expression patterns of 4 representative genes UBD, CUL3, HDAC6, and GADD45A were verified by quantitative real-time polymerase chain reaction and showed consistency with the microarray assay.
Conclusion:
Bortezomib could suppress cell viability, cause G2/M arrest, and induce apoptosis in human esophageal cancer cells, with possible targets including UBD, CUL3, HDAC6, and GADD45A.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>30961474</pmid><doi>10.1177/1533033819842546</doi><orcidid>https://orcid.org/0000-0001-6245-7653</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Annexin V Apoptosis Apoptosis - drug effects Bortezomib Bortezomib - pharmacology Calcium (reticular) Carcinoma - drug therapy Carcinoma - genetics Carcinoma - pathology Cell cycle Cell Cycle Proteins - genetics Cell Line, Tumor Cell Proliferation - drug effects Cell Survival - drug effects Cell viability Cullin Proteins - genetics DNA microarrays Endoplasmic reticulum Epithelial cells Epithelial Cells - drug effects Esophageal cancer Esophageal carcinoma Esophageal Neoplasms - drug therapy Esophageal Neoplasms - genetics Esophageal Neoplasms - pathology Esophagus Flow Cytometry G2 Phase Cell Cycle Checkpoints - drug effects Gadd45A protein Gene Expression Regulation, Neoplastic - drug effects Genomes Histone Deacetylase 6 - genetics Humans Microarray Analysis mRNA Multiple myeloma Neoplasm Proteins - genetics Original Polymerase chain reaction Propidium iodide Proteasomes RNA, Messenger - genetics Solid tumors Targeted cancer therapy Tumor cell lines Ubiquitins - genetics Wnt protein Wnt Signaling Pathway - drug effects |
| title | Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells |
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