Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa‐miR‐29b‐3p in pancreatic ductal adenocarcinoma
Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. Long non‐coding RNAs (lncRNAs) are important regulators in pathological processes, yet their potential roles in PDAC are poorly understood. Here, we identify a fundamental role for a novel lincRNA, linc00511, in the progression of PDAC....
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2018-01, Vol.22 (1), p.655-667 |
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| creator | Zhao, Xiaohui Liu, Yimin Li, Zhihua Zheng, Shangyou Wang, Zairui Li, Wenzhu Bi, Zhuofei Li, Liting Jiang, Yanhui Luo, Yuming Lin, Qing Fu, Zhiqiang Rufu, Chen |
| description | Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. Long non‐coding RNAs (lncRNAs) are important regulators in pathological processes, yet their potential roles in PDAC are poorly understood. Here, we identify a fundamental role for a novel lincRNA, linc00511, in the progression of PDAC. Linc00511 levels in PDAC tissue specimens and cell lines were examined by quantitative real‐time PCR. Corresponding adjacent non‐neoplastic tissues were used as controls. The function of linc00511 in PDAC cell lines was determined by RNA interference approach in vitro and in vivo. Fluorescence in situ hybridization (FISH) was used to characterize linc00511 expression in PDAC cells. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were obtained from bioinformatic analysis, luciferase assays and RIP assays. The association between the linc00511/hsa‐miR29b‐3p axis and VEGFA was verified by Western blotting assay. Immunohistochemistry was performed to evaluate the expression of VEGFA in PDAC samples. The aberrant up‐regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls. An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis. Functionally, linc00511 depletion in PDAC cells decreased proliferation, migration, invasion and endothelial tube formation. Mechanistically, linc00511 could up‐regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa‐miR‐29b‐3p. In summary, our results define an important axis controlling proliferation, invasion and tumour angiogenesis in PDAC. Linc00511 is a novel lncRNA that plays a significant regulatory role in the pathogenesis and progression of PDAC. Thus, Linc00511 represents a new prognostic biomarker to predict clinical outcome of PDAC patients after surgery and may serve as a potential therapeutic target for PDAC treatment. |
| doi_str_mv | 10.1111/jcmm.13351 |
| format | Article |
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Long non‐coding RNAs (lncRNAs) are important regulators in pathological processes, yet their potential roles in PDAC are poorly understood. Here, we identify a fundamental role for a novel lincRNA, linc00511, in the progression of PDAC. Linc00511 levels in PDAC tissue specimens and cell lines were examined by quantitative real‐time PCR. Corresponding adjacent non‐neoplastic tissues were used as controls. The function of linc00511 in PDAC cell lines was determined by RNA interference approach in vitro and in vivo. Fluorescence in situ hybridization (FISH) was used to characterize linc00511 expression in PDAC cells. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were obtained from bioinformatic analysis, luciferase assays and RIP assays. The association between the linc00511/hsa‐miR29b‐3p axis and VEGFA was verified by Western blotting assay. Immunohistochemistry was performed to evaluate the expression of VEGFA in PDAC samples. The aberrant up‐regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls. An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis. Functionally, linc00511 depletion in PDAC cells decreased proliferation, migration, invasion and endothelial tube formation. Mechanistically, linc00511 could up‐regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa‐miR‐29b‐3p. In summary, our results define an important axis controlling proliferation, invasion and tumour angiogenesis in PDAC. Linc00511 is a novel lncRNA that plays a significant regulatory role in the pathogenesis and progression of PDAC. Thus, Linc00511 represents a new prognostic biomarker to predict clinical outcome of PDAC patients after surgery and may serve as a potential therapeutic target for PDAC treatment.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.13351</identifier><identifier>PMID: 28984028</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adenocarcinoma ; Adenocarcinoma - blood supply ; Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Angiogenesis ; Animal tissues ; Assaying ; Base Sequence ; Carcinoma, Pancreatic Ductal - blood supply ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - pathology ; Cell Line, Tumor ; Cell lines ; Cell migration ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; Competing endogenous RNA ; Disease Progression ; Female ; Fluorescence ; Fluorescence in situ hybridization ; Gene Expression Regulation, Neoplastic ; hsa‐miR‐29b‐3p ; Humans ; Immunohistochemistry ; linc00511 ; Male ; Malignancy ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; Multivariate Analysis ; Neoplasm Invasiveness ; Neovascularization, Pathologic - genetics ; Original ; Pancreas ; Pancreatic cancer ; Pancreatic ductal adenocarcinoma ; Pancreatic Neoplasms ; Pancreatic Neoplasms - blood supply ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Prognosis ; Proportional Hazards Models ; Regulators ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; RNA-mediated interference ; Surgery ; Tumors ; Up-Regulation - genetics ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - metabolism ; VEGFA ; Western blotting</subject><ispartof>Journal of cellular and molecular medicine, 2018-01, Vol.22 (1), p.655-667</ispartof><rights>2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2018. This work is published 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4481-e639510c78147d109bb89dfc9393330ab24214a14a35dc9a4fe77aa576eb36603</citedby><cites>FETCH-LOGICAL-c4481-e639510c78147d109bb89dfc9393330ab24214a14a35dc9a4fe77aa576eb36603</cites><orcidid>0000-0002-8050-3243</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/PMC5742682/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5742682/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28984028$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Xiaohui</creatorcontrib><creatorcontrib>Liu, Yimin</creatorcontrib><creatorcontrib>Li, Zhihua</creatorcontrib><creatorcontrib>Zheng, Shangyou</creatorcontrib><creatorcontrib>Wang, Zairui</creatorcontrib><creatorcontrib>Li, Wenzhu</creatorcontrib><creatorcontrib>Bi, Zhuofei</creatorcontrib><creatorcontrib>Li, Liting</creatorcontrib><creatorcontrib>Jiang, Yanhui</creatorcontrib><creatorcontrib>Luo, Yuming</creatorcontrib><creatorcontrib>Lin, Qing</creatorcontrib><creatorcontrib>Fu, Zhiqiang</creatorcontrib><creatorcontrib>Rufu, Chen</creatorcontrib><title>Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa‐miR‐29b‐3p in pancreatic ductal adenocarcinoma</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. Long non‐coding RNAs (lncRNAs) are important regulators in pathological processes, yet their potential roles in PDAC are poorly understood. Here, we identify a fundamental role for a novel lincRNA, linc00511, in the progression of PDAC. Linc00511 levels in PDAC tissue specimens and cell lines were examined by quantitative real‐time PCR. Corresponding adjacent non‐neoplastic tissues were used as controls. The function of linc00511 in PDAC cell lines was determined by RNA interference approach in vitro and in vivo. Fluorescence in situ hybridization (FISH) was used to characterize linc00511 expression in PDAC cells. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were obtained from bioinformatic analysis, luciferase assays and RIP assays. The association between the linc00511/hsa‐miR29b‐3p axis and VEGFA was verified by Western blotting assay. Immunohistochemistry was performed to evaluate the expression of VEGFA in PDAC samples. The aberrant up‐regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls. An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis. Functionally, linc00511 depletion in PDAC cells decreased proliferation, migration, invasion and endothelial tube formation. Mechanistically, linc00511 could up‐regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa‐miR‐29b‐3p. In summary, our results define an important axis controlling proliferation, invasion and tumour angiogenesis in PDAC. Linc00511 is a novel lncRNA that plays a significant regulatory role in the pathogenesis and progression of PDAC. Thus, Linc00511 represents a new prognostic biomarker to predict clinical outcome of PDAC patients after surgery and may serve as a potential therapeutic target for PDAC treatment.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - blood supply</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Angiogenesis</subject><subject>Animal tissues</subject><subject>Assaying</subject><subject>Base Sequence</subject><subject>Carcinoma, Pancreatic Ductal - blood supply</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell lines</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Competing endogenous RNA</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Fluorescence</subject><subject>Fluorescence in situ hybridization</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>hsa‐miR‐29b‐3p</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>linc00511</subject><subject>Male</subject><subject>Malignancy</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>Multivariate Analysis</subject><subject>Neoplasm Invasiveness</subject><subject>Neovascularization, Pathologic - genetics</subject><subject>Original</subject><subject>Pancreas</subject><subject>Pancreatic cancer</subject><subject>Pancreatic ductal adenocarcinoma</subject><subject>Pancreatic Neoplasms</subject><subject>Pancreatic Neoplasms - blood supply</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Prognosis</subject><subject>Proportional Hazards Models</subject><subject>Regulators</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>RNA-mediated interference</subject><subject>Surgery</subject><subject>Tumors</subject><subject>Up-Regulation - genetics</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>VEGFA</subject><subject>Western blotting</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kdFqFDEUhgex2Fq98QEk4I0IW5NJZia5EZalrS1bhaLehjOZs7NZZpJpMqP2zkcQfEOfxGx3LeqF4fAnkC9_TvJn2TNGT1garzem708Y5wV7kB2xQuYzobh4uF8zyeVh9jjGDaW8ZFw9yg5zqaSguTzKfiytM5QWjBEwYySQihjfDzha1xJ0jW_R-SmS63dzMnoSsJ06GJF8Oj0_mxP8OgSM0XpHxnXwU7smcfCu3R5eR_j57Xtvr5Pmqk7KB2IdGcCZgDBaQ5rJjNARaNIdBoKxzvfwJDtYQRfx6X4-zj6enX5YvJ0t359fLObLmRFCshmWXBWMmkoyUTWMqrqWqlkZxRXnnEKdi5wJSMWLxigQK6wqgKIqseZlSflx9mbnO0x1j41BNwbo9BBsD-FWe7D67x1n17r1n3VRibyUeTJ4uTcI_mbCOOreRoNdBw7Tl2mmhKyKilVb9MU_6MZPwaXnJUpSoZLIRL3aUSb4GAOu7pthVG-z1tus9V3WCX7-Z_v36O9wE8B2wBfb4e1_rPTl4upqZ_oLzMa3tg</recordid><startdate>201801</startdate><enddate>201801</enddate><creator>Zhao, Xiaohui</creator><creator>Liu, Yimin</creator><creator>Li, Zhihua</creator><creator>Zheng, Shangyou</creator><creator>Wang, Zairui</creator><creator>Li, Wenzhu</creator><creator>Bi, Zhuofei</creator><creator>Li, Liting</creator><creator>Jiang, Yanhui</creator><creator>Luo, Yuming</creator><creator>Lin, Qing</creator><creator>Fu, Zhiqiang</creator><creator>Rufu, Chen</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8050-3243</orcidid></search><sort><creationdate>201801</creationdate><title>Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa‐miR‐29b‐3p in pancreatic ductal adenocarcinoma</title><author>Zhao, Xiaohui ; Liu, Yimin ; Li, Zhihua ; Zheng, Shangyou ; Wang, Zairui ; Li, Wenzhu ; Bi, Zhuofei ; Li, Liting ; Jiang, Yanhui ; Luo, Yuming ; Lin, Qing ; Fu, Zhiqiang ; Rufu, Chen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4481-e639510c78147d109bb89dfc9393330ab24214a14a35dc9a4fe77aa576eb36603</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - blood supply</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Angiogenesis</topic><topic>Animal tissues</topic><topic>Assaying</topic><topic>Base Sequence</topic><topic>Carcinoma, Pancreatic Ductal - blood supply</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell lines</topic><topic>Cell migration</topic><topic>Cell Movement - genetics</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Competing endogenous RNA</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Fluorescence</topic><topic>Fluorescence in situ hybridization</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>hsa‐miR‐29b‐3p</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>linc00511</topic><topic>Male</topic><topic>Malignancy</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>Multivariate Analysis</topic><topic>Neoplasm Invasiveness</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Original</topic><topic>Pancreas</topic><topic>Pancreatic cancer</topic><topic>Pancreatic ductal adenocarcinoma</topic><topic>Pancreatic Neoplasms</topic><topic>Pancreatic Neoplasms - blood supply</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Prognosis</topic><topic>Proportional Hazards Models</topic><topic>Regulators</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>RNA-mediated interference</topic><topic>Surgery</topic><topic>Tumors</topic><topic>Up-Regulation - genetics</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>VEGFA</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Xiaohui</creatorcontrib><creatorcontrib>Liu, Yimin</creatorcontrib><creatorcontrib>Li, Zhihua</creatorcontrib><creatorcontrib>Zheng, Shangyou</creatorcontrib><creatorcontrib>Wang, Zairui</creatorcontrib><creatorcontrib>Li, Wenzhu</creatorcontrib><creatorcontrib>Bi, Zhuofei</creatorcontrib><creatorcontrib>Li, Liting</creatorcontrib><creatorcontrib>Jiang, Yanhui</creatorcontrib><creatorcontrib>Luo, Yuming</creatorcontrib><creatorcontrib>Lin, Qing</creatorcontrib><creatorcontrib>Fu, Zhiqiang</creatorcontrib><creatorcontrib>Rufu, Chen</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library Free Content</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Xiaohui</au><au>Liu, Yimin</au><au>Li, Zhihua</au><au>Zheng, Shangyou</au><au>Wang, Zairui</au><au>Li, Wenzhu</au><au>Bi, Zhuofei</au><au>Li, Liting</au><au>Jiang, Yanhui</au><au>Luo, Yuming</au><au>Lin, Qing</au><au>Fu, Zhiqiang</au><au>Rufu, Chen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa‐miR‐29b‐3p in pancreatic ductal adenocarcinoma</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2018-01</date><risdate>2018</risdate><volume>22</volume><issue>1</issue><spage>655</spage><epage>667</epage><pages>655-667</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. Long non‐coding RNAs (lncRNAs) are important regulators in pathological processes, yet their potential roles in PDAC are poorly understood. Here, we identify a fundamental role for a novel lincRNA, linc00511, in the progression of PDAC. Linc00511 levels in PDAC tissue specimens and cell lines were examined by quantitative real‐time PCR. Corresponding adjacent non‐neoplastic tissues were used as controls. The function of linc00511 in PDAC cell lines was determined by RNA interference approach in vitro and in vivo. Fluorescence in situ hybridization (FISH) was used to characterize linc00511 expression in PDAC cells. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were obtained from bioinformatic analysis, luciferase assays and RIP assays. The association between the linc00511/hsa‐miR29b‐3p axis and VEGFA was verified by Western blotting assay. Immunohistochemistry was performed to evaluate the expression of VEGFA in PDAC samples. The aberrant up‐regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls. An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis. Functionally, linc00511 depletion in PDAC cells decreased proliferation, migration, invasion and endothelial tube formation. Mechanistically, linc00511 could up‐regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa‐miR‐29b‐3p. In summary, our results define an important axis controlling proliferation, invasion and tumour angiogenesis in PDAC. Linc00511 is a novel lncRNA that plays a significant regulatory role in the pathogenesis and progression of PDAC. Thus, Linc00511 represents a new prognostic biomarker to predict clinical outcome of PDAC patients after surgery and may serve as a potential therapeutic target for PDAC treatment.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>28984028</pmid><doi>10.1111/jcmm.13351</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-8050-3243</orcidid><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5742682 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Access via Wiley Online Library; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Adenocarcinoma Adenocarcinoma - blood supply Adenocarcinoma - genetics Adenocarcinoma - pathology Angiogenesis Animal tissues Assaying Base Sequence Carcinoma, Pancreatic Ductal - blood supply Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Cell Line, Tumor Cell lines Cell migration Cell Movement - genetics Cell proliferation Cell Proliferation - genetics Competing endogenous RNA Disease Progression Female Fluorescence Fluorescence in situ hybridization Gene Expression Regulation, Neoplastic hsa‐miR‐29b‐3p Humans Immunohistochemistry linc00511 Male Malignancy MicroRNAs - genetics MicroRNAs - metabolism Middle Aged Multivariate Analysis Neoplasm Invasiveness Neovascularization, Pathologic - genetics Original Pancreas Pancreatic cancer Pancreatic ductal adenocarcinoma Pancreatic Neoplasms Pancreatic Neoplasms - blood supply Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Prognosis Proportional Hazards Models Regulators RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA-mediated interference Surgery Tumors Up-Regulation - genetics Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism VEGFA Western blotting |
| title | Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa‐miR‐29b‐3p in pancreatic ductal adenocarcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-21T13%3A49%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Linc00511%20acts%20as%20a%20competing%20endogenous%20RNA%20to%20regulate%20VEGFA%20expression%20through%20sponging%20hsa%E2%80%90miR%E2%80%9029b%E2%80%903p%20in%20pancreatic%20ductal%20adenocarcinoma&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Zhao,%20Xiaohui&rft.date=2018-01&rft.volume=22&rft.issue=1&rft.spage=655&rft.epage=667&rft.pages=655-667&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.13351&rft_dat=%3Cproquest_pubme%3E1948757172%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1980499808&rft_id=info:pmid/28984028&rfr_iscdi=true |