LINC00958 promotes the proliferation of TSCC via miR-211-5p/CENPK axis and activating the JAK/STAT3 signaling pathway
Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown. The effect of LINC00...
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| Veröffentlicht in: | Cancer Cell International 2021-03, Vol.21 (1), p.147-147, Article 147 |
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| creator | Jia, Bo Dao, Junfeng Han, Jiusong Huang, Zhijie Sun, Xiang Zheng, Xianghuai Xiang, Shijian Zhou, Huixi Liu, Shuguang |
| description | Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown.
The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2'-deoxyuridline (EdU) assay and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays.
LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling.
Our findings suggested that LINC00958 is a potential prognostic biomarker in TSCC. |
| doi_str_mv | 10.1186/s12935-021-01808-z |
| format | Article |
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The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2'-deoxyuridline (EdU) assay and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays.
LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling.
Our findings suggested that LINC00958 is a potential prognostic biomarker in TSCC.</description><identifier>ISSN: 1475-2867</identifier><identifier>EISSN: 1475-2867</identifier><identifier>DOI: 10.1186/s12935-021-01808-z</identifier><identifier>PMID: 33658048</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Binding sites ; Bioinformatics ; Care and treatment ; Cell cycle ; Cell growth ; Cell proliferation ; CENPK ; Cholecystokinin ; Chromosome 5 ; Development and progression ; Flow cytometry ; Gene expression ; Genetic aspects ; Growth rate ; Health aspects ; Immunoprecipitation ; LINC00958 ; Liver cancer ; Medical prognosis ; MicroRNAs ; miR-211-5p ; Oncogenes ; Oral cancer ; Pancreatic cancer ; Primary Research ; Proliferation ; Proteins ; Signal transduction ; Software ; Squamous cell carcinoma ; Stat3 protein ; Surgery ; Tongue cancer ; TSCC ; Tumors ; Xenografts</subject><ispartof>Cancer Cell International, 2021-03, Vol.21 (1), p.147-147, Article 147</ispartof><rights>COPYRIGHT 2021 BioMed Central Ltd.</rights><rights>2021. 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>The Author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c663t-5c9695fdc5429d4d5d82ae2947bd830fd4d41ea4f7dbae58f21616efc7b351463</citedby><cites>FETCH-LOGICAL-c663t-5c9695fdc5429d4d5d82ae2947bd830fd4d41ea4f7dbae58f21616efc7b351463</cites><orcidid>0000-0003-0066-1020</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/PMC7931557/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7931557/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33658048$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jia, Bo</creatorcontrib><creatorcontrib>Dao, Junfeng</creatorcontrib><creatorcontrib>Han, Jiusong</creatorcontrib><creatorcontrib>Huang, Zhijie</creatorcontrib><creatorcontrib>Sun, Xiang</creatorcontrib><creatorcontrib>Zheng, Xianghuai</creatorcontrib><creatorcontrib>Xiang, Shijian</creatorcontrib><creatorcontrib>Zhou, Huixi</creatorcontrib><creatorcontrib>Liu, Shuguang</creatorcontrib><title>LINC00958 promotes the proliferation of TSCC via miR-211-5p/CENPK axis and activating the JAK/STAT3 signaling pathway</title><title>Cancer Cell International</title><addtitle>Cancer Cell Int</addtitle><description>Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown.
The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2'-deoxyuridline (EdU) assay and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays.
LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling.
Our findings suggested that LINC00958 is a potential prognostic biomarker in TSCC.</description><subject>Binding sites</subject><subject>Bioinformatics</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>CENPK</subject><subject>Cholecystokinin</subject><subject>Chromosome 5</subject><subject>Development and progression</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Growth rate</subject><subject>Health aspects</subject><subject>Immunoprecipitation</subject><subject>LINC00958</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>MicroRNAs</subject><subject>miR-211-5p</subject><subject>Oncogenes</subject><subject>Oral cancer</subject><subject>Pancreatic cancer</subject><subject>Primary Research</subject><subject>Proliferation</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Software</subject><subject>Squamous cell carcinoma</subject><subject>Stat3 protein</subject><subject>Surgery</subject><subject>Tongue cancer</subject><subject>TSCC</subject><subject>Tumors</subject><subject>Xenografts</subject><issn>1475-2867</issn><issn>1475-2867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>DOA</sourceid><recordid>eNpdUstuEzEAXCEQLYUf4IBW4sJlG7_tvSBFq1JCo4JoOFuOH4mj3XWwN6Ht1-NNStUiH2yPZ8Yea4riPQTnEAo2SRDVmFYAwQpAAUR1_6I4hYTTCgnGXz5ZnxRvUtoAALlg4HVxgjGjAhBxWuzms-sGgJqKchtDFwabymFtx03rnY1q8KEvgysXN01T7r0qO_-zQhBWdDtpLq5_XJXq1qdS9aZUevD7LOhXB4tv06vJzWK6wGXyq161I75Vw_qPuntbvHKqTfbdw3xW_PpysWi-VvPvl7NmOq80Y3ioqK5ZTZ3RlKDaEEONQMqimvClERi4DBFoFXHcLJWlwiHIILNO8yWmkDB8VsyOviaojdxG36l4J4Py8gCEuJIqDl63VkJtgCHcqNoB4vLNwlqjltkYCK0czF6fj17b3bKzRtt-iKp9Zvr8pPdruQp7yWsMKeXZ4NODQQy_dzYNsvNJ27ZVvQ27JBGpOeAC85H68T_qJuxi_sPMogDVY7gx3fmRtVI5gO9dyPfqPIztvA69dT7jU0YpQpwKnAXoKNAxpBSte3w9BHKslDxWSuZKyUOl5H0WfXia-1Hyr0P4L20Uxho</recordid><startdate>20210303</startdate><enddate>20210303</enddate><creator>Jia, Bo</creator><creator>Dao, Junfeng</creator><creator>Han, Jiusong</creator><creator>Huang, Zhijie</creator><creator>Sun, Xiang</creator><creator>Zheng, Xianghuai</creator><creator>Xiang, Shijian</creator><creator>Zhou, Huixi</creator><creator>Liu, Shuguang</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IAO</scope><scope>3V.</scope><scope>7TM</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><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-0066-1020</orcidid></search><sort><creationdate>20210303</creationdate><title>LINC00958 promotes the proliferation of TSCC via miR-211-5p/CENPK axis and activating the JAK/STAT3 signaling pathway</title><author>Jia, Bo ; Dao, Junfeng ; Han, Jiusong ; Huang, Zhijie ; Sun, Xiang ; Zheng, Xianghuai ; Xiang, Shijian ; Zhou, Huixi ; Liu, Shuguang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c663t-5c9695fdc5429d4d5d82ae2947bd830fd4d41ea4f7dbae58f21616efc7b351463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Binding sites</topic><topic>Bioinformatics</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>CENPK</topic><topic>Cholecystokinin</topic><topic>Chromosome 5</topic><topic>Development and progression</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Growth rate</topic><topic>Health aspects</topic><topic>Immunoprecipitation</topic><topic>LINC00958</topic><topic>Liver cancer</topic><topic>Medical prognosis</topic><topic>MicroRNAs</topic><topic>miR-211-5p</topic><topic>Oncogenes</topic><topic>Oral cancer</topic><topic>Pancreatic cancer</topic><topic>Primary Research</topic><topic>Proliferation</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Software</topic><topic>Squamous cell carcinoma</topic><topic>Stat3 protein</topic><topic>Surgery</topic><topic>Tongue cancer</topic><topic>TSCC</topic><topic>Tumors</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jia, Bo</creatorcontrib><creatorcontrib>Dao, Junfeng</creatorcontrib><creatorcontrib>Han, Jiusong</creatorcontrib><creatorcontrib>Huang, Zhijie</creatorcontrib><creatorcontrib>Sun, Xiang</creatorcontrib><creatorcontrib>Zheng, Xianghuai</creatorcontrib><creatorcontrib>Xiang, Shijian</creatorcontrib><creatorcontrib>Zhou, Huixi</creatorcontrib><creatorcontrib>Liu, Shuguang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</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><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cancer Cell International</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jia, Bo</au><au>Dao, Junfeng</au><au>Han, Jiusong</au><au>Huang, Zhijie</au><au>Sun, Xiang</au><au>Zheng, Xianghuai</au><au>Xiang, Shijian</au><au>Zhou, Huixi</au><au>Liu, Shuguang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LINC00958 promotes the proliferation of TSCC via miR-211-5p/CENPK axis and activating the JAK/STAT3 signaling pathway</atitle><jtitle>Cancer Cell International</jtitle><addtitle>Cancer Cell Int</addtitle><date>2021-03-03</date><risdate>2021</risdate><volume>21</volume><issue>1</issue><spage>147</spage><epage>147</epage><pages>147-147</pages><artnum>147</artnum><issn>1475-2867</issn><eissn>1475-2867</eissn><abstract>Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown.
The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2'-deoxyuridline (EdU) assay and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays.
LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling.
Our findings suggested that LINC00958 is a potential prognostic biomarker in TSCC.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>33658048</pmid><doi>10.1186/s12935-021-01808-z</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-0066-1020</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Binding sites Bioinformatics Care and treatment Cell cycle Cell growth Cell proliferation CENPK Cholecystokinin Chromosome 5 Development and progression Flow cytometry Gene expression Genetic aspects Growth rate Health aspects Immunoprecipitation LINC00958 Liver cancer Medical prognosis MicroRNAs miR-211-5p Oncogenes Oral cancer Pancreatic cancer Primary Research Proliferation Proteins Signal transduction Software Squamous cell carcinoma Stat3 protein Surgery Tongue cancer TSCC Tumors Xenografts |
| title | LINC00958 promotes the proliferation of TSCC via miR-211-5p/CENPK axis and activating the JAK/STAT3 signaling pathway |
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