CircLIFR Inhibits Non-small Cell Lung Cancer Progression by Acting as a miR-429 Sponge to Enhance CELF2 Expression
Lung cancer is the most commonly diagnosed cancer and the leading reason for tumor-related mortality, while non-small cell lung cancer (NSCLC) is the most usual type of lung cancer. Circular RNAs (circRNAs) have emerged as vital regulators in the development of human cancers, including NSCLC. We aim...
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| Veröffentlicht in: | Biochemical genetics 2023-04, Vol.61 (2), p.725-741 |
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| description | Lung cancer is the most commonly diagnosed cancer and the leading reason for tumor-related mortality, while non-small cell lung cancer (NSCLC) is the most usual type of lung cancer. Circular RNAs (circRNAs) have emerged as vital regulators in the development of human cancers, including NSCLC. We aimed to explore the functions of circRNA leukemia inhibitory factor receptor (circLIFR) in NSCLC progression. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to quantify the expression of circLIFR, microRNA-429 (miR-429), and Elav-like family member 2 (CELF2) in NSCLC tissues and cells. Cell proliferation capability of NSCLC cells was determined by Cell Counting Kit-8 (CCK-8) and colony formation assays. The flow cytometry assay was performed to evaluate cell-cycle distribution and apoptosis of NSCLC cells. The abilities of migration and invasion were measured by transwell assay. In addition, the activities of caspase 3 and caspase 9 were measured by the assay kits. The interaction relationship between miR-429 and circLIFR or CELF2 was analyzed by dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. The expression levels of related proteins were examined by Western Blot assay. The xenograft experiment was established to explore the role of circLIFR in vivo. CircLIFR, circular, and stable transcript in NSCLC cells, was decreased more than 2 folds in NSCLC tissues and cells than controls (
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| doi_str_mv | 10.1007/s10528-022-10285-6 |
| format | Article |
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P
< 0.0001). Importantly, overexpression of circLIFR impeded cell proliferation, migration, invasion, and inactivated protein kinase B (AKT)/phosphatase and tensin homolog (PTEN)-signaling pathways while enhanced apoptosis and cell-cycle arrest in NSCLC cells, which was overturned by upregulation of miR-429 or silencing of CELF2. Furthermore, the upregulation of circLIFR inhibited NSCLC tumor growth in vivo. Overexpression of circLIFR could suppress NSCLC progress by acting as a sponge of miR-429 to regulate the expression of CELF2 and PTEN/AKT-signaling pathways in NSCLC.</description><identifier>ISSN: 0006-2928</identifier><identifier>EISSN: 1573-4927</identifier><identifier>DOI: 10.1007/s10528-022-10285-6</identifier><identifier>PMID: 36104590</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>AKT protein ; Apoptosis ; Assaying ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Carcinoma, Non-Small-Cell Lung - genetics ; Caspase-3 ; Caspase-9 ; CELF Proteins ; Cell growth ; Cell migration ; Cell Proliferation ; Cholecystokinin ; Flow cytometry ; Gene expression ; Human Genetics ; Humans ; Immunoprecipitation ; Kinases ; Leukemia ; Leukemia inhibitory factor ; Leukemia Inhibitory Factor Receptor alpha Subunit - genetics ; Lung cancer ; Lung Neoplasms - genetics ; Medical Microbiology ; MicroRNAs - genetics ; miRNA ; Nerve Tissue Proteins ; Non-small cell lung carcinoma ; Original Article ; Polymerase chain reaction ; Proteins ; Proto-Oncogene Proteins c-akt ; PTEN protein ; Ribonucleic acid ; RNA ; Signal transduction ; Signaling ; Small cell lung carcinoma ; Tumors ; Xenografts ; Xenotransplantation ; Zoology</subject><ispartof>Biochemical genetics, 2023-04, Vol.61 (2), p.725-741</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-3726171f03005cd28950f0261b21620aac86e54c2cfd88048064fa5faf83d8dc3</citedby><cites>FETCH-LOGICAL-c375t-3726171f03005cd28950f0261b21620aac86e54c2cfd88048064fa5faf83d8dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10528-022-10285-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10528-022-10285-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36104590$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Junbin</creatorcontrib><creatorcontrib>Lai, Xinyi</creatorcontrib><creatorcontrib>Peng, Xuxing</creatorcontrib><title>CircLIFR Inhibits Non-small Cell Lung Cancer Progression by Acting as a miR-429 Sponge to Enhance CELF2 Expression</title><title>Biochemical genetics</title><addtitle>Biochem Genet</addtitle><addtitle>Biochem Genet</addtitle><description>Lung cancer is the most commonly diagnosed cancer and the leading reason for tumor-related mortality, while non-small cell lung cancer (NSCLC) is the most usual type of lung cancer. Circular RNAs (circRNAs) have emerged as vital regulators in the development of human cancers, including NSCLC. We aimed to explore the functions of circRNA leukemia inhibitory factor receptor (circLIFR) in NSCLC progression. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to quantify the expression of circLIFR, microRNA-429 (miR-429), and Elav-like family member 2 (CELF2) in NSCLC tissues and cells. Cell proliferation capability of NSCLC cells was determined by Cell Counting Kit-8 (CCK-8) and colony formation assays. The flow cytometry assay was performed to evaluate cell-cycle distribution and apoptosis of NSCLC cells. The abilities of migration and invasion were measured by transwell assay. In addition, the activities of caspase 3 and caspase 9 were measured by the assay kits. The interaction relationship between miR-429 and circLIFR or CELF2 was analyzed by dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. The expression levels of related proteins were examined by Western Blot assay. The xenograft experiment was established to explore the role of circLIFR in vivo. CircLIFR, circular, and stable transcript in NSCLC cells, was decreased more than 2 folds in NSCLC tissues and cells than controls (
P
< 0.0001). Importantly, overexpression of circLIFR impeded cell proliferation, migration, invasion, and inactivated protein kinase B (AKT)/phosphatase and tensin homolog (PTEN)-signaling pathways while enhanced apoptosis and cell-cycle arrest in NSCLC cells, which was overturned by upregulation of miR-429 or silencing of CELF2. Furthermore, the upregulation of circLIFR inhibited NSCLC tumor growth in vivo. Overexpression of circLIFR could suppress NSCLC progress by acting as a sponge of miR-429 to regulate the expression of CELF2 and PTEN/AKT-signaling pathways in NSCLC.</description><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Assaying</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>CELF Proteins</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell Proliferation</subject><subject>Cholecystokinin</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Leukemia inhibitory factor</subject><subject>Leukemia Inhibitory Factor Receptor alpha Subunit - genetics</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Medical Microbiology</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Nerve Tissue Proteins</subject><subject>Non-small cell lung carcinoma</subject><subject>Original Article</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>PTEN protein</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Small cell lung carcinoma</subject><subject>Tumors</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><subject>Zoology</subject><issn>0006-2928</issn><issn>1573-4927</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><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>eNp9kc1uEzEUhS0EomnhBVggS2zYGK7_PctqlNBII0AF1pbj8aRTZexgz0j07XFJAIkFG1v2_c7xvT4IvaLwjgLo94WCZIYAY4QCM5KoJ2hFpeZENEw_RSsAUIQ1zFygy1Lu67EBIZ6jC64oCNnACuV2zL7bbm7xNt6Nu3Eu-GOKpEzucMBtqEu3xD1uXfQh48857XMoZUwR7x7wtZ_HWnQFOzyNt0SwBn85prgPeE54He8eVbhddxuG1z-OZ-UL9GxwhxJenvcr9G2z_trekO7Th2173RHPtZwJ10xRTQfgANL3zDQSBqh3O0YVA-e8UUEKz_zQGwPCgBKDk4MbDO9N7_kVenvyPeb0fQllttNYfB3JxZCWYpmmQkneAK_om3_Q-7TkWLurVMOoVkzpSrET5XMqJYfBHvM4ufxgKdjHROwpEVsTsb8SsaqKXp-tl90U-j-S3xFUgJ-AUkv16_Lft_9j-xMLsJLQ</recordid><startdate>20230401</startdate><enddate>20230401</enddate><creator>Wang, Junbin</creator><creator>Lai, Xinyi</creator><creator>Peng, Xuxing</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7SS</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</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>C1K</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>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20230401</creationdate><title>CircLIFR Inhibits Non-small Cell Lung Cancer Progression by Acting as a miR-429 Sponge to Enhance CELF2 Expression</title><author>Wang, Junbin ; Lai, Xinyi ; Peng, Xuxing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-3726171f03005cd28950f0261b21620aac86e54c2cfd88048064fa5faf83d8dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>AKT protein</topic><topic>Apoptosis</topic><topic>Assaying</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Caspase-3</topic><topic>Caspase-9</topic><topic>CELF Proteins</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell Proliferation</topic><topic>Cholecystokinin</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Leukemia inhibitory factor</topic><topic>Leukemia Inhibitory Factor Receptor alpha Subunit - genetics</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Medical Microbiology</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Nerve Tissue Proteins</topic><topic>Non-small cell lung carcinoma</topic><topic>Original Article</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>PTEN protein</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Small cell lung carcinoma</topic><topic>Tumors</topic><topic>Xenografts</topic><topic>Xenotransplantation</topic><topic>Zoology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Junbin</creatorcontrib><creatorcontrib>Lai, Xinyi</creatorcontrib><creatorcontrib>Peng, Xuxing</creatorcontrib><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>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical 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>Environmental Sciences and Pollution Management</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>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Junbin</au><au>Lai, Xinyi</au><au>Peng, Xuxing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CircLIFR Inhibits Non-small Cell Lung Cancer Progression by Acting as a miR-429 Sponge to Enhance CELF2 Expression</atitle><jtitle>Biochemical genetics</jtitle><stitle>Biochem Genet</stitle><addtitle>Biochem Genet</addtitle><date>2023-04-01</date><risdate>2023</risdate><volume>61</volume><issue>2</issue><spage>725</spage><epage>741</epage><pages>725-741</pages><issn>0006-2928</issn><eissn>1573-4927</eissn><abstract>Lung cancer is the most commonly diagnosed cancer and the leading reason for tumor-related mortality, while non-small cell lung cancer (NSCLC) is the most usual type of lung cancer. Circular RNAs (circRNAs) have emerged as vital regulators in the development of human cancers, including NSCLC. We aimed to explore the functions of circRNA leukemia inhibitory factor receptor (circLIFR) in NSCLC progression. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to quantify the expression of circLIFR, microRNA-429 (miR-429), and Elav-like family member 2 (CELF2) in NSCLC tissues and cells. Cell proliferation capability of NSCLC cells was determined by Cell Counting Kit-8 (CCK-8) and colony formation assays. The flow cytometry assay was performed to evaluate cell-cycle distribution and apoptosis of NSCLC cells. The abilities of migration and invasion were measured by transwell assay. In addition, the activities of caspase 3 and caspase 9 were measured by the assay kits. The interaction relationship between miR-429 and circLIFR or CELF2 was analyzed by dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. The expression levels of related proteins were examined by Western Blot assay. The xenograft experiment was established to explore the role of circLIFR in vivo. CircLIFR, circular, and stable transcript in NSCLC cells, was decreased more than 2 folds in NSCLC tissues and cells than controls (
P
< 0.0001). Importantly, overexpression of circLIFR impeded cell proliferation, migration, invasion, and inactivated protein kinase B (AKT)/phosphatase and tensin homolog (PTEN)-signaling pathways while enhanced apoptosis and cell-cycle arrest in NSCLC cells, which was overturned by upregulation of miR-429 or silencing of CELF2. Furthermore, the upregulation of circLIFR inhibited NSCLC tumor growth in vivo. Overexpression of circLIFR could suppress NSCLC progress by acting as a sponge of miR-429 to regulate the expression of CELF2 and PTEN/AKT-signaling pathways in NSCLC.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36104590</pmid><doi>10.1007/s10528-022-10285-6</doi><tpages>17</tpages></addata></record> |
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| subjects | AKT protein Apoptosis Assaying Biochemistry Biomedical and Life Sciences Biomedicine Carcinoma, Non-Small-Cell Lung - genetics Caspase-3 Caspase-9 CELF Proteins Cell growth Cell migration Cell Proliferation Cholecystokinin Flow cytometry Gene expression Human Genetics Humans Immunoprecipitation Kinases Leukemia Leukemia inhibitory factor Leukemia Inhibitory Factor Receptor alpha Subunit - genetics Lung cancer Lung Neoplasms - genetics Medical Microbiology MicroRNAs - genetics miRNA Nerve Tissue Proteins Non-small cell lung carcinoma Original Article Polymerase chain reaction Proteins Proto-Oncogene Proteins c-akt PTEN protein Ribonucleic acid RNA Signal transduction Signaling Small cell lung carcinoma Tumors Xenografts Xenotransplantation Zoology |
| title | CircLIFR Inhibits Non-small Cell Lung Cancer Progression by Acting as a miR-429 Sponge to Enhance CELF2 Expression |
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