Knockdown of Ubiquitin-Specific Protease 14 (USP14) Inhibits the Proliferation and Tumorigenesis in Esophageal Squamous Cell Carcinoma Cells
Ubiquitin-specific protease 14 (USP14), one of three proteasome-associated deubiquitinating enzymes (DUBs), plays an essential role in the development of human carcinoma. However, to the best of our knowledge, the role of USP14 in esophageal squamous cell carcinoma (ESCC) is unknown. In the current...
Gespeichert in:
Veröffentlicht in: | Oncology research 2017-01, Vol.25 (2), p.249-257 |
---|---|
Hauptverfasser: | , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 257 |
---|---|
container_issue | 2 |
container_start_page | 249 |
container_title | Oncology research |
container_volume | 25 |
creator | Zhang, Jin Zhang, Danjie Sun, Liangzhang |
description | Ubiquitin-specific protease 14 (USP14), one of three proteasome-associated deubiquitinating enzymes (DUBs), plays an essential role in the development of human carcinoma. However, to the best of our knowledge, the role of USP14 in esophageal squamous cell carcinoma (ESCC) is unknown.
In the current study, we investigated the expression and role of USP14 in ESCC. Our results showed that the level of USP14 was significantly increased in ESCC tissues and cell lines. Downregulation of USP14 significantly inhibited ESCC cell proliferation and ESCC tumor growth in nude mice.
Downregulation of USP14 also suppressed the migration/invasion in ESCC cells. Mechanically, downregulation of USP14 decreased the protein expression levels of β-catenin, cyclin D1, and c-Myc in ESCC cells. In conclusion, our study shows that USP14 plays an important role in the progression
and metastasis of ESCC. Therefore, these data suggest that USP14 may be a potentially useful therapeutic strategy for the treatment of ESCC. |
doi_str_mv | 10.3727/096504016X693164 |
format | Article |
fullrecord | <record><control><sourceid>pubtec_pubme</sourceid><recordid>TN_cdi_pubmed_primary_27629392</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><ingid>cog/or/2017/00000025/00000002/art00011</ingid><sourcerecordid>cog/or/2017/00000025/00000002/art00011</sourcerecordid><originalsourceid>FETCH-LOGICAL-c522t-4cdff60fb21518d7e0b8573010b0c0f6e8f51a2ffd2382b577bc47b73cd868ec3</originalsourceid><addsrcrecordid>eNp1kU9vFCEYxonR2G317slw1MMoMDDMXEzMptbGRptsN_FGgIFZ6gxsganRz-CHlt2u9U8ilxfy8Px4eF8AnmH0quaEv0ZdwxBFuPncdDVu6AOwwIyxqu5Q8xAsdnJVdH4EjlO6RohQTrvH4IjwhnR1Rxbgxwcf9Jc-fPUwWLhW7mZ22flqtTXaWafhZQzZyGQgpvDFenWJ6Ut47jdOuZxg3pjdhdFZE2V2wUPpe3g1TyG6wXiTXILOw9MUths5GDnC1c0spzAnuDTjCJcyaufDJPfH9AQ8snJM5umhnoD1u9Or5fvq4tPZ-fLtRaUZIbmiure2QVYRzHDbc4NUy3iNMFJII9uY1jIsibU9qVuiGOdKU654rfu2aY2uT8CbO-52VpPptfE5ylFso5tk_CaCdOJvxbuNGMKt4C1FLWYFgO4AOoaUorH3XozEbjLi38kUy_M_37w3_BrF71DOl9ZlKa7DHH1pg9BhECEKgnDh7hdhhw0iQsZcKsYF8PE_AKf3jEMmLm4J86TwCC6_QSUzbUVvrJzHLLKMYvguUgH-BIwSuTE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Knockdown of Ubiquitin-Specific Protease 14 (USP14) Inhibits the Proliferation and Tumorigenesis in Esophageal Squamous Cell Carcinoma Cells</title><source>MEDLINE</source><source>IngentaConnect Open Access</source><source>PubMed Central</source><source>EZB Electronic Journals Library</source><source>PubMed Central Open Access</source><creator>Zhang, Jin ; Zhang, Danjie ; Sun, Liangzhang</creator><creatorcontrib>Zhang, Jin ; Zhang, Danjie ; Sun, Liangzhang</creatorcontrib><description>Ubiquitin-specific protease 14 (USP14), one of three proteasome-associated deubiquitinating enzymes (DUBs), plays an essential role in the development of human carcinoma. However, to the best of our knowledge, the role of USP14 in esophageal squamous cell carcinoma (ESCC) is unknown.
In the current study, we investigated the expression and role of USP14 in ESCC. Our results showed that the level of USP14 was significantly increased in ESCC tissues and cell lines. Downregulation of USP14 significantly inhibited ESCC cell proliferation and ESCC tumor growth in nude mice.
Downregulation of USP14 also suppressed the migration/invasion in ESCC cells. Mechanically, downregulation of USP14 decreased the protein expression levels of β-catenin, cyclin D1, and c-Myc in ESCC cells. In conclusion, our study shows that USP14 plays an important role in the progression
and metastasis of ESCC. Therefore, these data suggest that USP14 may be a potentially useful therapeutic strategy for the treatment of ESCC.</description><identifier>ISSN: 0965-0407</identifier><identifier>EISSN: 1555-3906</identifier><identifier>DOI: 10.3727/096504016X693164</identifier><identifier>PMID: 27629392</identifier><language>eng</language><publisher>Elmsford, NY: Cognizant Communication Corporation</publisher><subject>Animals ; Carcinogenesis - genetics ; Carcinogenesis - metabolism ; Carcinogenesis - pathology ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Cell Line, Tumor ; Cell Proliferation - physiology ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - metabolism ; Esophageal Neoplasms - pathology ; Esophageal Squamous Cell Carcinoma ; Esophageal Squamous Cell Carcinoma (escc) ; Female ; Gene Knockdown Techniques - methods ; Humans ; Invasion ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Proliferation ; Ubiquitin Thiolesterase - deficiency ; Ubiquitin Thiolesterase - genetics ; Ubiquitin Thiolesterase - metabolism ; Ubiquitin-Specific Protease 14 (usp14) ; Xenograft Model Antitumor Assays - methods</subject><ispartof>Oncology research, 2017-01, Vol.25 (2), p.249-257</ispartof><rights>Copyright © 2017 Cognizant, LLC. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c522t-4cdff60fb21518d7e0b8573010b0c0f6e8f51a2ffd2382b577bc47b73cd868ec3</citedby><cites>FETCH-LOGICAL-c522t-4cdff60fb21518d7e0b8573010b0c0f6e8f51a2ffd2382b577bc47b73cd868ec3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7840815/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7840815/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,288,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27629392$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Jin</creatorcontrib><creatorcontrib>Zhang, Danjie</creatorcontrib><creatorcontrib>Sun, Liangzhang</creatorcontrib><title>Knockdown of Ubiquitin-Specific Protease 14 (USP14) Inhibits the Proliferation and Tumorigenesis in Esophageal Squamous Cell Carcinoma Cells</title><title>Oncology research</title><addtitle>Oncol Res</addtitle><description>Ubiquitin-specific protease 14 (USP14), one of three proteasome-associated deubiquitinating enzymes (DUBs), plays an essential role in the development of human carcinoma. However, to the best of our knowledge, the role of USP14 in esophageal squamous cell carcinoma (ESCC) is unknown.
In the current study, we investigated the expression and role of USP14 in ESCC. Our results showed that the level of USP14 was significantly increased in ESCC tissues and cell lines. Downregulation of USP14 significantly inhibited ESCC cell proliferation and ESCC tumor growth in nude mice.
Downregulation of USP14 also suppressed the migration/invasion in ESCC cells. Mechanically, downregulation of USP14 decreased the protein expression levels of β-catenin, cyclin D1, and c-Myc in ESCC cells. In conclusion, our study shows that USP14 plays an important role in the progression
and metastasis of ESCC. Therefore, these data suggest that USP14 may be a potentially useful therapeutic strategy for the treatment of ESCC.</description><subject>Animals</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - metabolism</subject><subject>Carcinogenesis - pathology</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - physiology</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - metabolism</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophageal Squamous Cell Carcinoma</subject><subject>Esophageal Squamous Cell Carcinoma (escc)</subject><subject>Female</subject><subject>Gene Knockdown Techniques - methods</subject><subject>Humans</subject><subject>Invasion</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Proliferation</subject><subject>Ubiquitin Thiolesterase - deficiency</subject><subject>Ubiquitin Thiolesterase - genetics</subject><subject>Ubiquitin Thiolesterase - metabolism</subject><subject>Ubiquitin-Specific Protease 14 (usp14)</subject><subject>Xenograft Model Antitumor Assays - methods</subject><issn>0965-0407</issn><issn>1555-3906</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU9vFCEYxonR2G317slw1MMoMDDMXEzMptbGRptsN_FGgIFZ6gxsganRz-CHlt2u9U8ilxfy8Px4eF8AnmH0quaEv0ZdwxBFuPncdDVu6AOwwIyxqu5Q8xAsdnJVdH4EjlO6RohQTrvH4IjwhnR1Rxbgxwcf9Jc-fPUwWLhW7mZ22flqtTXaWafhZQzZyGQgpvDFenWJ6Ut47jdOuZxg3pjdhdFZE2V2wUPpe3g1TyG6wXiTXILOw9MUths5GDnC1c0spzAnuDTjCJcyaufDJPfH9AQ8snJM5umhnoD1u9Or5fvq4tPZ-fLtRaUZIbmiure2QVYRzHDbc4NUy3iNMFJII9uY1jIsibU9qVuiGOdKU654rfu2aY2uT8CbO-52VpPptfE5ylFso5tk_CaCdOJvxbuNGMKt4C1FLWYFgO4AOoaUorH3XozEbjLi38kUy_M_37w3_BrF71DOl9ZlKa7DHH1pg9BhECEKgnDh7hdhhw0iQsZcKsYF8PE_AKf3jEMmLm4J86TwCC6_QSUzbUVvrJzHLLKMYvguUgH-BIwSuTE</recordid><startdate>20170126</startdate><enddate>20170126</enddate><creator>Zhang, Jin</creator><creator>Zhang, Danjie</creator><creator>Sun, Liangzhang</creator><general>Cognizant Communication Corporation</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>5PM</scope></search><sort><creationdate>20170126</creationdate><title>Knockdown of Ubiquitin-Specific Protease 14 (USP14) Inhibits the Proliferation and Tumorigenesis in Esophageal Squamous Cell Carcinoma Cells</title><author>Zhang, Jin ; Zhang, Danjie ; Sun, Liangzhang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c522t-4cdff60fb21518d7e0b8573010b0c0f6e8f51a2ffd2382b577bc47b73cd868ec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - metabolism</topic><topic>Carcinogenesis - pathology</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - physiology</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - metabolism</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophageal Squamous Cell Carcinoma</topic><topic>Esophageal Squamous Cell Carcinoma (escc)</topic><topic>Female</topic><topic>Gene Knockdown Techniques - methods</topic><topic>Humans</topic><topic>Invasion</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Proliferation</topic><topic>Ubiquitin Thiolesterase - deficiency</topic><topic>Ubiquitin Thiolesterase - genetics</topic><topic>Ubiquitin Thiolesterase - metabolism</topic><topic>Ubiquitin-Specific Protease 14 (usp14)</topic><topic>Xenograft Model Antitumor Assays - methods</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Jin</creatorcontrib><creatorcontrib>Zhang, Danjie</creatorcontrib><creatorcontrib>Sun, Liangzhang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Jin</au><au>Zhang, Danjie</au><au>Sun, Liangzhang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockdown of Ubiquitin-Specific Protease 14 (USP14) Inhibits the Proliferation and Tumorigenesis in Esophageal Squamous Cell Carcinoma Cells</atitle><jtitle>Oncology research</jtitle><addtitle>Oncol Res</addtitle><date>2017-01-26</date><risdate>2017</risdate><volume>25</volume><issue>2</issue><spage>249</spage><epage>257</epage><pages>249-257</pages><issn>0965-0407</issn><eissn>1555-3906</eissn><abstract>Ubiquitin-specific protease 14 (USP14), one of three proteasome-associated deubiquitinating enzymes (DUBs), plays an essential role in the development of human carcinoma. However, to the best of our knowledge, the role of USP14 in esophageal squamous cell carcinoma (ESCC) is unknown.
In the current study, we investigated the expression and role of USP14 in ESCC. Our results showed that the level of USP14 was significantly increased in ESCC tissues and cell lines. Downregulation of USP14 significantly inhibited ESCC cell proliferation and ESCC tumor growth in nude mice.
Downregulation of USP14 also suppressed the migration/invasion in ESCC cells. Mechanically, downregulation of USP14 decreased the protein expression levels of β-catenin, cyclin D1, and c-Myc in ESCC cells. In conclusion, our study shows that USP14 plays an important role in the progression
and metastasis of ESCC. Therefore, these data suggest that USP14 may be a potentially useful therapeutic strategy for the treatment of ESCC.</abstract><cop>Elmsford, NY</cop><pub>Cognizant Communication Corporation</pub><pmid>27629392</pmid><doi>10.3727/096504016X693164</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0965-0407 |
ispartof | Oncology research, 2017-01, Vol.25 (2), p.249-257 |
issn | 0965-0407 1555-3906 |
language | eng |
recordid | cdi_pubmed_primary_27629392 |
source | MEDLINE; IngentaConnect Open Access; PubMed Central; EZB Electronic Journals Library; PubMed Central Open Access |
subjects | Animals Carcinogenesis - genetics Carcinogenesis - metabolism Carcinogenesis - pathology Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Cell Line, Tumor Cell Proliferation - physiology Esophageal Neoplasms - genetics Esophageal Neoplasms - metabolism Esophageal Neoplasms - pathology Esophageal Squamous Cell Carcinoma Esophageal Squamous Cell Carcinoma (escc) Female Gene Knockdown Techniques - methods Humans Invasion Mice Mice, Inbred BALB C Mice, Nude Proliferation Ubiquitin Thiolesterase - deficiency Ubiquitin Thiolesterase - genetics Ubiquitin Thiolesterase - metabolism Ubiquitin-Specific Protease 14 (usp14) Xenograft Model Antitumor Assays - methods |
title | Knockdown of Ubiquitin-Specific Protease 14 (USP14) Inhibits the Proliferation and Tumorigenesis in Esophageal Squamous Cell Carcinoma Cells |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-11T17%3A06%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubtec_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Knockdown%20of%20Ubiquitin-Specific%20Protease%2014%20(USP14)%20Inhibits%20the%20Proliferation%20and%20Tumorigenesis%20in%20Esophageal%20Squamous%20Cell%20Carcinoma%20Cells&rft.jtitle=Oncology%20research&rft.au=Zhang,%20Jin&rft.date=2017-01-26&rft.volume=25&rft.issue=2&rft.spage=249&rft.epage=257&rft.pages=249-257&rft.issn=0965-0407&rft.eissn=1555-3906&rft_id=info:doi/10.3727/096504016X693164&rft_dat=%3Cpubtec_pubme%3Ecog/or/2017/00000025/00000002/art00011%3C/pubtec_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/27629392&rft_ingid=cog/or/2017/00000025/00000002/art00011&rfr_iscdi=true |