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Downregulation of Ubiquitin Inhibits the Aggressive Phenotypes of Esophageal Squamous Cell Carcinoma
Purpose: Esophageal cancer is one of the most common malignancies worldwide. Ubiquitin-dependent degradation of regulatory proteins reportedly plays a central role in diverse cellular processes. This study investigated the expression levels of ubiquitin in esophageal squamous cell carcinoma tissues...
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| Published in: | Technology in cancer research & treatment 2020, Vol.19, p.1533033820973282-1533033820973282 |
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| container_title | Technology in cancer research & treatment |
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| creator | Gao, Yi Mo, Wei Zhong, Li Jia, Huimin Xu, Yiren Zhang, Ji Xu, Xiaohui Shen, Weidong Wang, Fangjun Li, Tengfei Liu, Pengfei Zhang, Shuyu |
| description | Purpose:
Esophageal cancer is one of the most common malignancies worldwide. Ubiquitin-dependent degradation of regulatory proteins reportedly plays a central role in diverse cellular processes. This study investigated the expression levels of ubiquitin in esophageal squamous cell carcinoma tissues and the functions of ubiquitin in the context of esophageal squamous cell carcinoma progression.
Methods:
The expression of ubiquitin in esophageal squamous cell carcinoma and normal esophageal samples was determined via immunohistochemistry. Serum ubiquitin levels were determined by enzyme-linked immunosorbent assay. The association between serum ubiquitin level and clinicopathological factors was analyzed. Real-time PCR analysis was employed to measure the mRNA levels of the ubiquitin coding genes ubiquitin B and ubiquitin C. Proliferation assays, colony formation assays, and Transwell-based assays were used to determine the influence of ubiquitin on cell growth and cell invasion. Proteomic analysis was performed to identify the proteins associated with ubiquitin.
Results:
Ubiquitin expression in esophageal squamous cell carcinoma tissues was markedly higher than that in normal and tumor adjacent tissues. The levels of ubiquitin in esophageal squamous cell carcinoma serum samples were significantly higher than those in healthy controls. Serum ubiquitin levels were correlated with tumor stage and lymph node metastasis. To silence the expression of ubiquitin, we knocked down the ubiquitin coding genes ubiquitin B and ubiquitin C in TE-1 and Eca-109 cells. Silencing ubiquitin resulted in the suppression of cell growth, chemoresistance, colony formation and cell migration in esophageal squamous cell carcinoma cells. Proteomic analysis in esophageal squamous cell carcinoma cells showed that knockdown of ubiquitin coding genes deregulated the expression of 159 proteins (92 were upregulated and 67 were downregulated) involved in multiple pathways. These proteins included ferritin light chain, ferritin heavy chain, cellular retinoic acid-binding protein 2, and DNA replication factor 1.
Conclusion:
Ubiquitin expression is upregulated in esophageal squamous cell carcinoma tissues and serum samples. Serum ubiquitin levels were correlated with tumor stage and lymph node metastasis. Downregulation of ubiquitin suppresses the aggressive phenotypes of esophageal squamous cell carcinoma cells by complex mechanisms; ubiquitin may represent a novel target for the treatment of e |
| doi_str_mv | 10.1177/1533033820973282 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_7e41f3aece304fe1a653be9b544a70c2</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_1533033820973282</sage_id><doaj_id>oai_doaj_org_article_7e41f3aece304fe1a653be9b544a70c2</doaj_id><sourcerecordid>2460082106</sourcerecordid><originalsourceid>FETCH-LOGICAL-c528t-5a6298d9e9a1c144c0d903c8e04d9d37e68449e05442119288217d194f224cf03</originalsourceid><addsrcrecordid>eNp1kktv1DAUhSMEog_Ys0KW2LAJ-BU73iBVQ4GRKoEEXVuOc5N4lNgzdtKq_x5Ppwy0Et7YOj73s--jKN4Q_IEQKT-SijHMWE2xkozW9FlxupfKvfb8eObipDhLaYMxFYKRl8UJY0SKSpHTov0cbn2EfhnN7IJHoUPXjdstbnYerf3gGjcnNA-ALvo-QkruBtCPAXyY77aQ9v7LFLaD6cGM6OduMVNYElrBOKKVidb5MJlXxYvOjAleP-znxfWXy1-rb-XV96_r1cVVaStaz2VlBFV1q0AZYgnnFrcKM1sD5q1qmQRRc64AV5xTQhSta0pkSxTvKOW2w-y8WB-4bTAbvY1uMvFOB-P0vRBir02cnR1BS-CkYwYsMMw7IEZUrAHVZLaR2NLM-nRgbZdmgtaCn6MZH0Ef33g36D7caCkklRXPgPcPgBh2C6RZTy7ZXBfjIZdIUy4wzhlgka3vnlg3YYk-l0rTSqi8uJTZhQ8uG0NKEbrjZwjW-3HQT8chh7z9N4ljwJ_-Z0N5MKTcwL-v_hf4GwFhvJY</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2569999477</pqid></control><display><type>article</type><title>Downregulation of Ubiquitin Inhibits the Aggressive Phenotypes of Esophageal Squamous Cell Carcinoma</title><source>Publicly Available Content Database</source><source>Sage Journals GOLD Open Access 2024</source><source>PubMed Central</source><creator>Gao, Yi ; Mo, Wei ; Zhong, Li ; Jia, Huimin ; Xu, Yiren ; Zhang, Ji ; Xu, Xiaohui ; Shen, Weidong ; Wang, Fangjun ; Li, Tengfei ; Liu, Pengfei ; Zhang, Shuyu</creator><creatorcontrib>Gao, Yi ; Mo, Wei ; Zhong, Li ; Jia, Huimin ; Xu, Yiren ; Zhang, Ji ; Xu, Xiaohui ; Shen, Weidong ; Wang, Fangjun ; Li, Tengfei ; Liu, Pengfei ; Zhang, Shuyu</creatorcontrib><description>Purpose:
Esophageal cancer is one of the most common malignancies worldwide. Ubiquitin-dependent degradation of regulatory proteins reportedly plays a central role in diverse cellular processes. This study investigated the expression levels of ubiquitin in esophageal squamous cell carcinoma tissues and the functions of ubiquitin in the context of esophageal squamous cell carcinoma progression.
Methods:
The expression of ubiquitin in esophageal squamous cell carcinoma and normal esophageal samples was determined via immunohistochemistry. Serum ubiquitin levels were determined by enzyme-linked immunosorbent assay. The association between serum ubiquitin level and clinicopathological factors was analyzed. Real-time PCR analysis was employed to measure the mRNA levels of the ubiquitin coding genes ubiquitin B and ubiquitin C. Proliferation assays, colony formation assays, and Transwell-based assays were used to determine the influence of ubiquitin on cell growth and cell invasion. Proteomic analysis was performed to identify the proteins associated with ubiquitin.
Results:
Ubiquitin expression in esophageal squamous cell carcinoma tissues was markedly higher than that in normal and tumor adjacent tissues. The levels of ubiquitin in esophageal squamous cell carcinoma serum samples were significantly higher than those in healthy controls. Serum ubiquitin levels were correlated with tumor stage and lymph node metastasis. To silence the expression of ubiquitin, we knocked down the ubiquitin coding genes ubiquitin B and ubiquitin C in TE-1 and Eca-109 cells. Silencing ubiquitin resulted in the suppression of cell growth, chemoresistance, colony formation and cell migration in esophageal squamous cell carcinoma cells. Proteomic analysis in esophageal squamous cell carcinoma cells showed that knockdown of ubiquitin coding genes deregulated the expression of 159 proteins (92 were upregulated and 67 were downregulated) involved in multiple pathways. These proteins included ferritin light chain, ferritin heavy chain, cellular retinoic acid-binding protein 2, and DNA replication factor 1.
Conclusion:
Ubiquitin expression is upregulated in esophageal squamous cell carcinoma tissues and serum samples. Serum ubiquitin levels were correlated with tumor stage and lymph node metastasis. Downregulation of ubiquitin suppresses the aggressive phenotypes of esophageal squamous cell carcinoma cells by complex mechanisms; ubiquitin may represent a novel target for the treatment of esophageal squamous cell carcinoma.</description><identifier>ISSN: 1533-0346</identifier><identifier>EISSN: 1533-0338</identifier><identifier>DOI: 10.1177/1533033820973282</identifier><identifier>PMID: 33176591</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Cell growth ; Cell migration ; Chemoresistance ; Colonies ; DNA biosynthesis ; Enzyme-linked immunosorbent assay ; Esophageal cancer ; Esophagus ; Ferritin ; Immunohistochemistry ; Lymph nodes ; Lymphatic system ; Metastases ; Metastasis ; mRNA ; Original ; Phenotypes ; Proteins ; Regulatory proteins ; Retinoic acid ; Squamous cell carcinoma ; Ubiquitin</subject><ispartof>Technology in cancer research & treatment, 2020, Vol.19, p.1533033820973282-1533033820973282</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://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) 2020 2020 SAGE Publications</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-5a6298d9e9a1c144c0d903c8e04d9d37e68449e05442119288217d194f224cf03</citedby><cites>FETCH-LOGICAL-c528t-5a6298d9e9a1c144c0d903c8e04d9d37e68449e05442119288217d194f224cf03</cites><orcidid>0000-0001-7122-9126</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/PMC7672754/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2569999477?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,21945,25731,27830,27900,27901,27902,36989,36990,44566,44921,45309,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33176591$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Yi</creatorcontrib><creatorcontrib>Mo, Wei</creatorcontrib><creatorcontrib>Zhong, Li</creatorcontrib><creatorcontrib>Jia, Huimin</creatorcontrib><creatorcontrib>Xu, Yiren</creatorcontrib><creatorcontrib>Zhang, Ji</creatorcontrib><creatorcontrib>Xu, Xiaohui</creatorcontrib><creatorcontrib>Shen, Weidong</creatorcontrib><creatorcontrib>Wang, Fangjun</creatorcontrib><creatorcontrib>Li, Tengfei</creatorcontrib><creatorcontrib>Liu, Pengfei</creatorcontrib><creatorcontrib>Zhang, Shuyu</creatorcontrib><title>Downregulation of Ubiquitin Inhibits the Aggressive Phenotypes of Esophageal Squamous Cell Carcinoma</title><title>Technology in cancer research & treatment</title><addtitle>Technol Cancer Res Treat</addtitle><description>Purpose:
Esophageal cancer is one of the most common malignancies worldwide. Ubiquitin-dependent degradation of regulatory proteins reportedly plays a central role in diverse cellular processes. This study investigated the expression levels of ubiquitin in esophageal squamous cell carcinoma tissues and the functions of ubiquitin in the context of esophageal squamous cell carcinoma progression.
Methods:
The expression of ubiquitin in esophageal squamous cell carcinoma and normal esophageal samples was determined via immunohistochemistry. Serum ubiquitin levels were determined by enzyme-linked immunosorbent assay. The association between serum ubiquitin level and clinicopathological factors was analyzed. Real-time PCR analysis was employed to measure the mRNA levels of the ubiquitin coding genes ubiquitin B and ubiquitin C. Proliferation assays, colony formation assays, and Transwell-based assays were used to determine the influence of ubiquitin on cell growth and cell invasion. Proteomic analysis was performed to identify the proteins associated with ubiquitin.
Results:
Ubiquitin expression in esophageal squamous cell carcinoma tissues was markedly higher than that in normal and tumor adjacent tissues. The levels of ubiquitin in esophageal squamous cell carcinoma serum samples were significantly higher than those in healthy controls. Serum ubiquitin levels were correlated with tumor stage and lymph node metastasis. To silence the expression of ubiquitin, we knocked down the ubiquitin coding genes ubiquitin B and ubiquitin C in TE-1 and Eca-109 cells. Silencing ubiquitin resulted in the suppression of cell growth, chemoresistance, colony formation and cell migration in esophageal squamous cell carcinoma cells. Proteomic analysis in esophageal squamous cell carcinoma cells showed that knockdown of ubiquitin coding genes deregulated the expression of 159 proteins (92 were upregulated and 67 were downregulated) involved in multiple pathways. These proteins included ferritin light chain, ferritin heavy chain, cellular retinoic acid-binding protein 2, and DNA replication factor 1.
Conclusion:
Ubiquitin expression is upregulated in esophageal squamous cell carcinoma tissues and serum samples. Serum ubiquitin levels were correlated with tumor stage and lymph node metastasis. Downregulation of ubiquitin suppresses the aggressive phenotypes of esophageal squamous cell carcinoma cells by complex mechanisms; ubiquitin may represent a novel target for the treatment of esophageal squamous cell carcinoma.</description><subject>Cell growth</subject><subject>Cell migration</subject><subject>Chemoresistance</subject><subject>Colonies</subject><subject>DNA biosynthesis</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Esophageal cancer</subject><subject>Esophagus</subject><subject>Ferritin</subject><subject>Immunohistochemistry</subject><subject>Lymph nodes</subject><subject>Lymphatic system</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>mRNA</subject><subject>Original</subject><subject>Phenotypes</subject><subject>Proteins</subject><subject>Regulatory proteins</subject><subject>Retinoic acid</subject><subject>Squamous cell carcinoma</subject><subject>Ubiquitin</subject><issn>1533-0346</issn><issn>1533-0338</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp1kktv1DAUhSMEog_Ys0KW2LAJ-BU73iBVQ4GRKoEEXVuOc5N4lNgzdtKq_x5Ppwy0Et7YOj73s--jKN4Q_IEQKT-SijHMWE2xkozW9FlxupfKvfb8eObipDhLaYMxFYKRl8UJY0SKSpHTov0cbn2EfhnN7IJHoUPXjdstbnYerf3gGjcnNA-ALvo-QkruBtCPAXyY77aQ9v7LFLaD6cGM6OduMVNYElrBOKKVidb5MJlXxYvOjAleP-znxfWXy1-rb-XV96_r1cVVaStaz2VlBFV1q0AZYgnnFrcKM1sD5q1qmQRRc64AV5xTQhSta0pkSxTvKOW2w-y8WB-4bTAbvY1uMvFOB-P0vRBir02cnR1BS-CkYwYsMMw7IEZUrAHVZLaR2NLM-nRgbZdmgtaCn6MZH0Ef33g36D7caCkklRXPgPcPgBh2C6RZTy7ZXBfjIZdIUy4wzhlgka3vnlg3YYk-l0rTSqi8uJTZhQ8uG0NKEbrjZwjW-3HQT8chh7z9N4ljwJ_-Z0N5MKTcwL-v_hf4GwFhvJY</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Gao, Yi</creator><creator>Mo, Wei</creator><creator>Zhong, Li</creator><creator>Jia, Huimin</creator><creator>Xu, Yiren</creator><creator>Zhang, Ji</creator><creator>Xu, Xiaohui</creator><creator>Shen, Weidong</creator><creator>Wang, Fangjun</creator><creator>Li, Tengfei</creator><creator>Liu, Pengfei</creator><creator>Zhang, Shuyu</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><general>SAGE Publishing</general><scope>AFRWT</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>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-7122-9126</orcidid></search><sort><creationdate>2020</creationdate><title>Downregulation of Ubiquitin Inhibits the Aggressive Phenotypes of Esophageal Squamous Cell Carcinoma</title><author>Gao, Yi ; Mo, Wei ; Zhong, Li ; Jia, Huimin ; Xu, Yiren ; Zhang, Ji ; Xu, Xiaohui ; Shen, Weidong ; Wang, Fangjun ; Li, Tengfei ; Liu, Pengfei ; Zhang, Shuyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-5a6298d9e9a1c144c0d903c8e04d9d37e68449e05442119288217d194f224cf03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Cell growth</topic><topic>Cell migration</topic><topic>Chemoresistance</topic><topic>Colonies</topic><topic>DNA biosynthesis</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Esophageal cancer</topic><topic>Esophagus</topic><topic>Ferritin</topic><topic>Immunohistochemistry</topic><topic>Lymph nodes</topic><topic>Lymphatic system</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>mRNA</topic><topic>Original</topic><topic>Phenotypes</topic><topic>Proteins</topic><topic>Regulatory proteins</topic><topic>Retinoic acid</topic><topic>Squamous cell carcinoma</topic><topic>Ubiquitin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Yi</creatorcontrib><creatorcontrib>Mo, Wei</creatorcontrib><creatorcontrib>Zhong, Li</creatorcontrib><creatorcontrib>Jia, Huimin</creatorcontrib><creatorcontrib>Xu, Yiren</creatorcontrib><creatorcontrib>Zhang, Ji</creatorcontrib><creatorcontrib>Xu, Xiaohui</creatorcontrib><creatorcontrib>Shen, Weidong</creatorcontrib><creatorcontrib>Wang, Fangjun</creatorcontrib><creatorcontrib>Li, Tengfei</creatorcontrib><creatorcontrib>Liu, Pengfei</creatorcontrib><creatorcontrib>Zhang, Shuyu</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</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)</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</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ: Directory of Open Access Journals</collection><jtitle>Technology in cancer research & treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Yi</au><au>Mo, Wei</au><au>Zhong, Li</au><au>Jia, Huimin</au><au>Xu, Yiren</au><au>Zhang, Ji</au><au>Xu, Xiaohui</au><au>Shen, Weidong</au><au>Wang, Fangjun</au><au>Li, Tengfei</au><au>Liu, Pengfei</au><au>Zhang, Shuyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulation of Ubiquitin Inhibits the Aggressive Phenotypes of Esophageal Squamous Cell Carcinoma</atitle><jtitle>Technology in cancer research & treatment</jtitle><addtitle>Technol Cancer Res Treat</addtitle><date>2020</date><risdate>2020</risdate><volume>19</volume><spage>1533033820973282</spage><epage>1533033820973282</epage><pages>1533033820973282-1533033820973282</pages><issn>1533-0346</issn><eissn>1533-0338</eissn><abstract>Purpose:
Esophageal cancer is one of the most common malignancies worldwide. Ubiquitin-dependent degradation of regulatory proteins reportedly plays a central role in diverse cellular processes. This study investigated the expression levels of ubiquitin in esophageal squamous cell carcinoma tissues and the functions of ubiquitin in the context of esophageal squamous cell carcinoma progression.
Methods:
The expression of ubiquitin in esophageal squamous cell carcinoma and normal esophageal samples was determined via immunohistochemistry. Serum ubiquitin levels were determined by enzyme-linked immunosorbent assay. The association between serum ubiquitin level and clinicopathological factors was analyzed. Real-time PCR analysis was employed to measure the mRNA levels of the ubiquitin coding genes ubiquitin B and ubiquitin C. Proliferation assays, colony formation assays, and Transwell-based assays were used to determine the influence of ubiquitin on cell growth and cell invasion. Proteomic analysis was performed to identify the proteins associated with ubiquitin.
Results:
Ubiquitin expression in esophageal squamous cell carcinoma tissues was markedly higher than that in normal and tumor adjacent tissues. The levels of ubiquitin in esophageal squamous cell carcinoma serum samples were significantly higher than those in healthy controls. Serum ubiquitin levels were correlated with tumor stage and lymph node metastasis. To silence the expression of ubiquitin, we knocked down the ubiquitin coding genes ubiquitin B and ubiquitin C in TE-1 and Eca-109 cells. Silencing ubiquitin resulted in the suppression of cell growth, chemoresistance, colony formation and cell migration in esophageal squamous cell carcinoma cells. Proteomic analysis in esophageal squamous cell carcinoma cells showed that knockdown of ubiquitin coding genes deregulated the expression of 159 proteins (92 were upregulated and 67 were downregulated) involved in multiple pathways. These proteins included ferritin light chain, ferritin heavy chain, cellular retinoic acid-binding protein 2, and DNA replication factor 1.
Conclusion:
Ubiquitin expression is upregulated in esophageal squamous cell carcinoma tissues and serum samples. Serum ubiquitin levels were correlated with tumor stage and lymph node metastasis. Downregulation of ubiquitin suppresses the aggressive phenotypes of esophageal squamous cell carcinoma cells by complex mechanisms; ubiquitin may represent a novel target for the treatment of esophageal squamous cell carcinoma.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>33176591</pmid><doi>10.1177/1533033820973282</doi><orcidid>https://orcid.org/0000-0001-7122-9126</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Publicly Available Content Database; Sage Journals GOLD Open Access 2024; PubMed Central |
| subjects | Cell growth Cell migration Chemoresistance Colonies DNA biosynthesis Enzyme-linked immunosorbent assay Esophageal cancer Esophagus Ferritin Immunohistochemistry Lymph nodes Lymphatic system Metastases Metastasis mRNA Original Phenotypes Proteins Regulatory proteins Retinoic acid Squamous cell carcinoma Ubiquitin |
| title | Downregulation of Ubiquitin Inhibits the Aggressive Phenotypes of Esophageal Squamous Cell Carcinoma |
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