miR‑1343‑3p inhibits autophagy by directly targeting ATG7 in multiple myeloma cells
Multiple myeloma (MM) is the second most common type of hematological malignancy globally. Despite application of several new drugs, such as daratumumab, bortezomib/lenalidomide/dexamethasone, in combination with hematopoietic stem cell transplantation, overall prognosis remains poor and the patholo...
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description | Multiple myeloma (MM) is the second most common type of hematological malignancy globally. Despite application of several new drugs, such as daratumumab, bortezomib/lenalidomide/dexamethasone, in combination with hematopoietic stem cell transplantation, overall prognosis remains poor and the pathological mechanism of MM is still unknown. The present study used TargetScan to predict autophagy-related 7 (ATG7) as a candidate target gene of microRNA (miR)-1343-3p and confirmed the interaction between miR-1343-3p and the ATG7 3' untranslated region (3'UTR) using a dual-luciferase reporter assay. In U266 and RPMI-8226 MM cell lines, miR-1343-3p mimic transfection decreased mRNA and protein levels of ATG7, while miR-1343-3p inhibition increased ATG7 expression levels using reverse transcription-qPCR and western blot analysis. miR-1343-3p mimic transfection inhibited U266 and RPMI-8226 cell survival. Finally, miR-1343-3p regulated ATG7 and autophagy in MM cells using western blot analysis. The present findings suggested that miR-1343-3p may regulate ATG7 and autophagy by directly targeting the 3'UTR of ATG7. To the best of our knowledge, there are no direct data showing the roles of miR-1343-3p in development of MM; however, miR-1343-3p may be considered a potential target for MM treatment. |
doi_str_mv | 10.3892/br.2024.1873 |
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Despite application of several new drugs, such as daratumumab, bortezomib/lenalidomide/dexamethasone, in combination with hematopoietic stem cell transplantation, overall prognosis remains poor and the pathological mechanism of MM is still unknown. The present study used TargetScan to predict autophagy-related 7 (ATG7) as a candidate target gene of microRNA (miR)-1343-3p and confirmed the interaction between miR-1343-3p and the ATG7 3' untranslated region (3'UTR) using a dual-luciferase reporter assay. In U266 and RPMI-8226 MM cell lines, miR-1343-3p mimic transfection decreased mRNA and protein levels of ATG7, while miR-1343-3p inhibition increased ATG7 expression levels using reverse transcription-qPCR and western blot analysis. miR-1343-3p mimic transfection inhibited U266 and RPMI-8226 cell survival. Finally, miR-1343-3p regulated ATG7 and autophagy in MM cells using western blot analysis. The present findings suggested that miR-1343-3p may regulate ATG7 and autophagy by directly targeting the 3'UTR of ATG7. To the best of our knowledge, there are no direct data showing the roles of miR-1343-3p in development of MM; however, miR-1343-3p may be considered a potential target for MM treatment.</description><identifier>ISSN: 2049-9434</identifier><identifier>ISSN: 2049-9442</identifier><identifier>EISSN: 2049-9442</identifier><identifier>DOI: 10.3892/br.2024.1873</identifier><identifier>PMID: 39420924</identifier><language>eng</language><publisher>England: Spandidos Publications</publisher><subject>3' Untranslated regions ; Apoptosis ; Autophagy ; B cells ; Biotechnology industry ; Bone marrow ; Bortezomib ; Cell culture ; Cell cycle ; Cell growth ; Cell survival ; Development and progression ; Dexamethasone ; Gene expression ; Genes ; Hematology ; Hematopoietic stem cells ; Immunosuppressive agents ; Infection ; Malignancy ; MicroRNA ; MicroRNAs ; miRNA ; Multiple myeloma ; Ovarian cancer ; Prognosis ; Proteins ; Reverse transcription ; Stem cell transplantation ; Stem cells ; Thyroid cancer ; Transfection ; Transplantation ; Tumors</subject><ispartof>Biomedical reports, 2024-12, Vol.21 (6), p.185, Article 185</ispartof><rights>Copyright: © 2024 Guo et al.</rights><rights>COPYRIGHT 2024 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2024</rights><rights>Copyright: © 2024 Guo et al. 2024</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c367t-4b09f0e7326544ea64ea790d40ff4e3d1b66c111b15966260e123342049fe3183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484188/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484188/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39420924$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Yanrong</creatorcontrib><creatorcontrib>Ding, Xiaoxiao</creatorcontrib><creatorcontrib>Dai, Changling</creatorcontrib><creatorcontrib>Wang, Wenwen</creatorcontrib><creatorcontrib>Chen, Jianlin</creatorcontrib><creatorcontrib>Chen, Sai</creatorcontrib><creatorcontrib>Yang, Linjun</creatorcontrib><creatorcontrib>Chen, Guang</creatorcontrib><title>miR‑1343‑3p inhibits autophagy by directly targeting ATG7 in multiple myeloma cells</title><title>Biomedical reports</title><addtitle>Biomed Rep</addtitle><description>Multiple myeloma (MM) is the second most common type of hematological malignancy globally. Despite application of several new drugs, such as daratumumab, bortezomib/lenalidomide/dexamethasone, in combination with hematopoietic stem cell transplantation, overall prognosis remains poor and the pathological mechanism of MM is still unknown. The present study used TargetScan to predict autophagy-related 7 (ATG7) as a candidate target gene of microRNA (miR)-1343-3p and confirmed the interaction between miR-1343-3p and the ATG7 3' untranslated region (3'UTR) using a dual-luciferase reporter assay. In U266 and RPMI-8226 MM cell lines, miR-1343-3p mimic transfection decreased mRNA and protein levels of ATG7, while miR-1343-3p inhibition increased ATG7 expression levels using reverse transcription-qPCR and western blot analysis. miR-1343-3p mimic transfection inhibited U266 and RPMI-8226 cell survival. Finally, miR-1343-3p regulated ATG7 and autophagy in MM cells using western blot analysis. The present findings suggested that miR-1343-3p may regulate ATG7 and autophagy by directly targeting the 3'UTR of ATG7. To the best of our knowledge, there are no direct data showing the roles of miR-1343-3p in development of MM; however, miR-1343-3p may be considered a potential target for MM treatment.</description><subject>3' Untranslated regions</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>B cells</subject><subject>Biotechnology industry</subject><subject>Bone marrow</subject><subject>Bortezomib</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell survival</subject><subject>Development and progression</subject><subject>Dexamethasone</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Hematology</subject><subject>Hematopoietic stem cells</subject><subject>Immunosuppressive agents</subject><subject>Infection</subject><subject>Malignancy</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Multiple myeloma</subject><subject>Ovarian cancer</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Reverse transcription</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Thyroid cancer</subject><subject>Transfection</subject><subject>Transplantation</subject><subject>Tumors</subject><issn>2049-9434</issn><issn>2049-9442</issn><issn>2049-9442</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptks9qFTEUxoNYbKnduZaAGxfea_5NJlnJpWgrFASpuAyZmTNzUzKTMZkpzM5X8BV9kmZovVppQjgh-Z3v8CUHoVeUbLnS7H0Vt4wwsaWq5M_QCSNCb7QQ7Plhz8UxOkvphuShS8IK9QIdcy0Y0UycoO-9-_r75y_KBc-Bj9gNe1e5KWE7T2Hc227B1YIbF6Ge_IInGzuY3NDh3fVFmWncz35yowfcL-BDb3EN3qeX6Ki1PsHZQzxF3z59vD6_3Fx9ufh8vrva1FyW00ZURLcESs5kIQRYmVepSSNI2wrgDa2krCmlFS20lEwSoIxzsXprgVPFT9GHe91xrnpoahimaL0Zo-ttXEywzjy-GdzedOHWUCqUoGpVePugEMOPGdJkepdWD3aAMCfDKS21VorJjL75D70Jcxyyv0yxgkgiS_2X6qwH44Y25ML1Kmp2ipZCEVqITG2foPJsoHd1GKB1-fxRwrv7hDqGlCK0B5OUmLUZTBXN2gxmbYaMv_73YQ7wn6_nd8FXrbo</recordid><startdate>20241201</startdate><enddate>20241201</enddate><creator>Guo, Yanrong</creator><creator>Ding, Xiaoxiao</creator><creator>Dai, Changling</creator><creator>Wang, Wenwen</creator><creator>Chen, Jianlin</creator><creator>Chen, Sai</creator><creator>Yang, Linjun</creator><creator>Chen, Guang</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20241201</creationdate><title>miR‑1343‑3p inhibits autophagy by directly targeting ATG7 in multiple myeloma cells</title><author>Guo, Yanrong ; Ding, Xiaoxiao ; Dai, Changling ; Wang, Wenwen ; Chen, Jianlin ; Chen, Sai ; Yang, Linjun ; Chen, Guang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c367t-4b09f0e7326544ea64ea790d40ff4e3d1b66c111b15966260e123342049fe3183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>3' Untranslated regions</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>B cells</topic><topic>Biotechnology industry</topic><topic>Bone marrow</topic><topic>Bortezomib</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell survival</topic><topic>Development and progression</topic><topic>Dexamethasone</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Hematology</topic><topic>Hematopoietic stem cells</topic><topic>Immunosuppressive agents</topic><topic>Infection</topic><topic>Malignancy</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Multiple myeloma</topic><topic>Ovarian cancer</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Reverse transcription</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Thyroid cancer</topic><topic>Transfection</topic><topic>Transplantation</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Guo, Yanrong</creatorcontrib><creatorcontrib>Ding, Xiaoxiao</creatorcontrib><creatorcontrib>Dai, Changling</creatorcontrib><creatorcontrib>Wang, Wenwen</creatorcontrib><creatorcontrib>Chen, Jianlin</creatorcontrib><creatorcontrib>Chen, Sai</creatorcontrib><creatorcontrib>Yang, Linjun</creatorcontrib><creatorcontrib>Chen, Guang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</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>Biomedical reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Yanrong</au><au>Ding, Xiaoxiao</au><au>Dai, Changling</au><au>Wang, Wenwen</au><au>Chen, Jianlin</au><au>Chen, Sai</au><au>Yang, Linjun</au><au>Chen, Guang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR‑1343‑3p inhibits autophagy by directly targeting ATG7 in multiple myeloma cells</atitle><jtitle>Biomedical reports</jtitle><addtitle>Biomed Rep</addtitle><date>2024-12-01</date><risdate>2024</risdate><volume>21</volume><issue>6</issue><spage>185</spage><pages>185-</pages><artnum>185</artnum><issn>2049-9434</issn><issn>2049-9442</issn><eissn>2049-9442</eissn><abstract>Multiple myeloma (MM) is the second most common type of hematological malignancy globally. Despite application of several new drugs, such as daratumumab, bortezomib/lenalidomide/dexamethasone, in combination with hematopoietic stem cell transplantation, overall prognosis remains poor and the pathological mechanism of MM is still unknown. The present study used TargetScan to predict autophagy-related 7 (ATG7) as a candidate target gene of microRNA (miR)-1343-3p and confirmed the interaction between miR-1343-3p and the ATG7 3' untranslated region (3'UTR) using a dual-luciferase reporter assay. In U266 and RPMI-8226 MM cell lines, miR-1343-3p mimic transfection decreased mRNA and protein levels of ATG7, while miR-1343-3p inhibition increased ATG7 expression levels using reverse transcription-qPCR and western blot analysis. miR-1343-3p mimic transfection inhibited U266 and RPMI-8226 cell survival. Finally, miR-1343-3p regulated ATG7 and autophagy in MM cells using western blot analysis. The present findings suggested that miR-1343-3p may regulate ATG7 and autophagy by directly targeting the 3'UTR of ATG7. To the best of our knowledge, there are no direct data showing the roles of miR-1343-3p in development of MM; however, miR-1343-3p may be considered a potential target for MM treatment.</abstract><cop>England</cop><pub>Spandidos Publications</pub><pmid>39420924</pmid><doi>10.3892/br.2024.1873</doi><oa>free_for_read</oa></addata></record> |
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subjects | 3' Untranslated regions Apoptosis Autophagy B cells Biotechnology industry Bone marrow Bortezomib Cell culture Cell cycle Cell growth Cell survival Development and progression Dexamethasone Gene expression Genes Hematology Hematopoietic stem cells Immunosuppressive agents Infection Malignancy MicroRNA MicroRNAs miRNA Multiple myeloma Ovarian cancer Prognosis Proteins Reverse transcription Stem cell transplantation Stem cells Thyroid cancer Transfection Transplantation Tumors |
title | miR‑1343‑3p inhibits autophagy by directly targeting ATG7 in multiple myeloma cells |
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