Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis
Background. Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined...
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description | Background. Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined the functional role and regulatory mechanism of WDFY3-AS2 in EC. Materials and Methods. RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells. The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN. Counting Clock Kit-8 (CCK-8) assay was carried out to detect cell viability, and transwell assays were used for measuring cell migration and invasion. Results. Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients. Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. Additionally, WDFY3-AS2 was negatively correlated with miR-18a and positively with PTEN. Furthermore, we discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression. Conclusions. WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC. |
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Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined the functional role and regulatory mechanism of WDFY3-AS2 in EC. Materials and Methods. RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells. The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN. Counting Clock Kit-8 (CCK-8) assay was carried out to detect cell viability, and transwell assays were used for measuring cell migration and invasion. Results. Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients. Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. Additionally, WDFY3-AS2 was negatively correlated with miR-18a and positively with PTEN. Furthermore, we discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression. Conclusions. WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC.</description><identifier>ISSN: 1687-8450</identifier><identifier>EISSN: 1687-8450</identifier><identifier>EISSN: 1687-8469</identifier><identifier>DOI: 10.1155/2021/9951010</identifier><identifier>PMID: 34194502</identifier><language>eng</language><publisher>Egypt: Hindawi</publisher><subject>Antisense RNA ; Binding sites ; Chemotherapy ; Development and progression ; Esophageal cancer ; Investigations ; Liver cancer ; Medical prognosis ; Medical research ; Medicine, Experimental ; Proteins ; Tumors</subject><ispartof>Journal of oncology, 2021, Vol.2021, p.9951010-12</ispartof><rights>Copyright © 2021 Qingling Kong et al.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>Copyright © 2021 Qingling Kong et al. This work is licensed under http://creativecommons.org/licenses/by/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>Copyright © 2021 Qingling Kong et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-c7aac515100479a29b6dc76dcc144951224b28d72c93e8ff9e32ecc9cb2d9b943</citedby><cites>FETCH-LOGICAL-c434t-c7aac515100479a29b6dc76dcc144951224b28d72c93e8ff9e32ecc9cb2d9b943</cites><orcidid>0000-0001-6133-1282</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/PMC8203383/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8203383/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34194502$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Yuchi, Alamgeer</contributor><contributor>Alamgeer Yuchi</contributor><creatorcontrib>Kong, Qingling</creatorcontrib><creatorcontrib>Li, Guangcai</creatorcontrib><creatorcontrib>Yin, Gang</creatorcontrib><creatorcontrib>Li, Kun</creatorcontrib><creatorcontrib>Zhang, Dongqing</creatorcontrib><creatorcontrib>Xu, Weihao</creatorcontrib><title>Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis</title><title>Journal of oncology</title><addtitle>J Oncol</addtitle><description>Background. Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined the functional role and regulatory mechanism of WDFY3-AS2 in EC. Materials and Methods. RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells. The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN. Counting Clock Kit-8 (CCK-8) assay was carried out to detect cell viability, and transwell assays were used for measuring cell migration and invasion. Results. Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients. Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. Additionally, WDFY3-AS2 was negatively correlated with miR-18a and positively with PTEN. Furthermore, we discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression. Conclusions. WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC.</description><subject>Antisense RNA</subject><subject>Binding sites</subject><subject>Chemotherapy</subject><subject>Development and progression</subject><subject>Esophageal cancer</subject><subject>Investigations</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Proteins</subject><subject>Tumors</subject><issn>1687-8450</issn><issn>1687-8450</issn><issn>1687-8469</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp9ks1v0zAYhyMEYmNw44wscZnEQv2Z2BekqOsAqSpTGUKcLMdxEk-pXexmg_9-jlrG4LCD5df2o8f62W-WvUbwPUKMzTDEaCYEQxDBJ9kxKniZc8rg0wf1UfYixmsICwpF8Tw7IhSJtI2PM7P0rgMr77RvbKrWqwp8P7_4QfLqKwZrsw0mRhPBrjfgMvhuWlrvgG_BIvptrzqjBjBXTpuQoODHrgcbu84RV7PLq8UKVL9sfJk9a9UQzavDfJJ9u1hczT_lyy8fP8-rZa4pobtcl0pphlIUSEuhsKiLRpdpaERpSogxrTFvSqwFMbxthSHYaC10jRtRC0pOsg9773asN6bRxu2CGuQ22I0Kv6VXVv574mwvO38jOYaEcJIEpwdB8D9HE3dyY6M2w6Cc8WOUmNGSEY4xS-jb_9BrPwaX4k0UwZBShP5SnRqMtK716V49SWVViIILiEnxOMUJ40kIE3W2p3TwMQbT3gdDUE69IKdekIdeSPibh49xD__5_AS82wO9dY26tY_r7gCm_7da</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Kong, Qingling</creator><creator>Li, Guangcai</creator><creator>Yin, Gang</creator><creator>Li, Kun</creator><creator>Zhang, Dongqing</creator><creator>Xu, Weihao</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</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>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</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/0000-0001-6133-1282</orcidid></search><sort><creationdate>2021</creationdate><title>Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis</title><author>Kong, Qingling ; Li, Guangcai ; Yin, Gang ; Li, Kun ; Zhang, Dongqing ; Xu, Weihao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-c7aac515100479a29b6dc76dcc144951224b28d72c93e8ff9e32ecc9cb2d9b943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antisense RNA</topic><topic>Binding sites</topic><topic>Chemotherapy</topic><topic>Development and progression</topic><topic>Esophageal cancer</topic><topic>Investigations</topic><topic>Liver cancer</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Proteins</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kong, Qingling</creatorcontrib><creatorcontrib>Li, Guangcai</creatorcontrib><creatorcontrib>Yin, Gang</creatorcontrib><creatorcontrib>Li, Kun</creatorcontrib><creatorcontrib>Zhang, Dongqing</creatorcontrib><creatorcontrib>Xu, Weihao</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>Access via ProQuest (Open Access)</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>Journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kong, Qingling</au><au>Li, Guangcai</au><au>Yin, Gang</au><au>Li, Kun</au><au>Zhang, Dongqing</au><au>Xu, Weihao</au><au>Yuchi, Alamgeer</au><au>Alamgeer Yuchi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis</atitle><jtitle>Journal of oncology</jtitle><addtitle>J Oncol</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><spage>9951010</spage><epage>12</epage><pages>9951010-12</pages><issn>1687-8450</issn><eissn>1687-8450</eissn><eissn>1687-8469</eissn><abstract>Background. Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined the functional role and regulatory mechanism of WDFY3-AS2 in EC. Materials and Methods. RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells. The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN. Counting Clock Kit-8 (CCK-8) assay was carried out to detect cell viability, and transwell assays were used for measuring cell migration and invasion. Results. Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients. Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. Additionally, WDFY3-AS2 was negatively correlated with miR-18a and positively with PTEN. Furthermore, we discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression. Conclusions. WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC.</abstract><cop>Egypt</cop><pub>Hindawi</pub><pmid>34194502</pmid><doi>10.1155/2021/9951010</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-6133-1282</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antisense RNA Binding sites Chemotherapy Development and progression Esophageal cancer Investigations Liver cancer Medical prognosis Medical research Medicine, Experimental Proteins Tumors |
title | Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis |
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