lncRNA MIAT promotes luminal B breast cancer cell proliferation, migration, and invasion in vitro
Long noncoding RNAs (lncRNAs) play a role in the emergence and progression of several human tumors, including luminal B breast cancer (BC). The biological functions and potential mechanisms of lncRNA myocardial infarction-associated transcripts (MIAT) in luminal B BC, on the contrary, are unknown. I...
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description | Long noncoding RNAs (lncRNAs) play a role in the emergence and progression of several human tumors, including luminal B breast cancer (BC). The biological functions and potential mechanisms of lncRNA myocardial infarction-associated transcripts (MIAT) in luminal B BC, on the contrary, are unknown. In this work, we used UALCAN database analysis to find high expression of lncRNA MIAT in luminal BC tissues and also confirmed high levels of lncRNA MIAT expression in luminal B BC tissues and cells. In vitro knockdown of MIAT inhibited the proliferation, migration, and invasion of BT474 cells. In addition, we found that miR-150-5p levels were significantly reduced in luminal B BC specimens and cells, and miR-150-5p levels were significantly increased when MIAT was knocked down. And TIMER database analysis showed that MIAT was positively associated with PDL1. Through bioinformatic tools and in vitro experiments, lncRNA MIAT could function as a competitive endogenous RNA (CeRNA) to further regulate programmed cell death ligand 1 (PDL1) expression by directly sponging miR-150-5p. In conclusion, our data suggest that MIAT, an oncogene, may sponge miR-150-5p to regulate PDL1 expression and affect proliferation, migration, and invasion in luminal B BC in vitro. |
doi_str_mv | 10.1007/s13353-023-00807-2 |
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The biological functions and potential mechanisms of lncRNA myocardial infarction-associated transcripts (MIAT) in luminal B BC, on the contrary, are unknown. In this work, we used UALCAN database analysis to find high expression of lncRNA MIAT in luminal BC tissues and also confirmed high levels of lncRNA MIAT expression in luminal B BC tissues and cells. In vitro knockdown of MIAT inhibited the proliferation, migration, and invasion of BT474 cells. In addition, we found that miR-150-5p levels were significantly reduced in luminal B BC specimens and cells, and miR-150-5p levels were significantly increased when MIAT was knocked down. And TIMER database analysis showed that MIAT was positively associated with PDL1. Through bioinformatic tools and in vitro experiments, lncRNA MIAT could function as a competitive endogenous RNA (CeRNA) to further regulate programmed cell death ligand 1 (PDL1) expression by directly sponging miR-150-5p. In conclusion, our data suggest that MIAT, an oncogene, may sponge miR-150-5p to regulate PDL1 expression and affect proliferation, migration, and invasion in luminal B BC in vitro.</description><identifier>ISSN: 1234-1983</identifier><identifier>EISSN: 2190-3883</identifier><identifier>DOI: 10.1007/s13353-023-00807-2</identifier><identifier>PMID: 37987972</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animal Genetics and Genomics ; Apoptosis ; bioinformatics ; Biomedical and Life Sciences ; Breast cancer ; breast neoplasms ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cell death ; Cell migration ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Human Genetics ; Human Genetics • Original Paper ; Humans ; Life Sciences ; ligands ; Microbial Genetics and Genomics ; MicroRNAs - genetics ; Myocardial infarction ; Myocardial Infarction - genetics ; neoplasm cells ; Non-coding RNA ; oncogenes ; Plant Genetics and Genomics ; programmed cell death ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism</subject><ispartof>Journal of applied genetics, 2024-05, Vol.65 (2), p.309-319</ispartof><rights>The Author(s), under exclusive licence to Institute of Plant Genetics Polish Academy of Sciences 2023. Springer Nature or its licensor (e.g. a society or other partner) 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>2023. The Author(s), under exclusive licence to Institute of Plant Genetics Polish Academy of Sciences.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c359t-978fdff14418a52a6332b6ae7fd7ffcef85a204de52962574abfbe8265e960ff3</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/s13353-023-00807-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13353-023-00807-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37987972$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mi, Jintao</creatorcontrib><creatorcontrib>Zhang, Hongsheng</creatorcontrib><creatorcontrib>Jiang, Xuemei</creatorcontrib><creatorcontrib>Yi, Ying</creatorcontrib><creatorcontrib>Cao, Weiwei</creatorcontrib><creatorcontrib>Song, Chunjiao</creatorcontrib><creatorcontrib>Yuan, Chengliang</creatorcontrib><title>lncRNA MIAT promotes luminal B breast cancer cell proliferation, migration, and invasion in vitro</title><title>Journal of applied genetics</title><addtitle>J Appl Genetics</addtitle><addtitle>J Appl Genet</addtitle><description>Long noncoding RNAs (lncRNAs) play a role in the emergence and progression of several human tumors, including luminal B breast cancer (BC). The biological functions and potential mechanisms of lncRNA myocardial infarction-associated transcripts (MIAT) in luminal B BC, on the contrary, are unknown. In this work, we used UALCAN database analysis to find high expression of lncRNA MIAT in luminal BC tissues and also confirmed high levels of lncRNA MIAT expression in luminal B BC tissues and cells. In vitro knockdown of MIAT inhibited the proliferation, migration, and invasion of BT474 cells. In addition, we found that miR-150-5p levels were significantly reduced in luminal B BC specimens and cells, and miR-150-5p levels were significantly increased when MIAT was knocked down. And TIMER database analysis showed that MIAT was positively associated with PDL1. Through bioinformatic tools and in vitro experiments, lncRNA MIAT could function as a competitive endogenous RNA (CeRNA) to further regulate programmed cell death ligand 1 (PDL1) expression by directly sponging miR-150-5p. In conclusion, our data suggest that MIAT, an oncogene, may sponge miR-150-5p to regulate PDL1 expression and affect proliferation, migration, and invasion in luminal B BC in vitro.</description><subject>Animal Genetics and Genomics</subject><subject>Apoptosis</subject><subject>bioinformatics</subject><subject>Biomedical and Life Sciences</subject><subject>Breast cancer</subject><subject>breast neoplasms</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell death</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Human Genetics</subject><subject>Human Genetics • Original Paper</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>ligands</subject><subject>Microbial Genetics and Genomics</subject><subject>MicroRNAs - genetics</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - genetics</subject><subject>neoplasm cells</subject><subject>Non-coding RNA</subject><subject>oncogenes</subject><subject>Plant Genetics and Genomics</subject><subject>programmed cell death</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><issn>1234-1983</issn><issn>2190-3883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1PxCAQhonR6PrxBzwYEi8erAIDhR7XjV_JqonRM6EtmJqWrtBu4r-Xdf1IPHiYMIRn3hnmReiQkjNKiDyPFEBARlgKoojM2AaaMFqQDJSCTTShDHhGCwU7aDfGV0JAccm20Q7IQslCsgkyra8e76f47nb6hBeh7_rBRtyOXeNNiy9wGayJA66Mr2zAlW3bFdU2zgYzNL0_xV3z8p0aX-PGL01Mt5TgZTOEfh9tOdNGe_B17qHnq8un2U02f7i-nU3nWQWiGLJCKlc7RzmnyghmcgBW5sZKV0vnKuuUMIzw2gpW5ExIbkpXWsVyYYucOAd76GStm-Z7G20cdNfE1cDG236MGqgASXPOeUKP_6Cv_RjShxNFQFAQSshEsTVVhT7GYJ1ehKYz4V1TolcG6LUBOhmgPw3QLBUdfUmPZWfrn5LvjScA1kBMT_7Fht_e_8h-AJxOkGY</recordid><startdate>20240501</startdate><enddate>20240501</enddate><creator>Mi, Jintao</creator><creator>Zhang, Hongsheng</creator><creator>Jiang, Xuemei</creator><creator>Yi, Ying</creator><creator>Cao, Weiwei</creator><creator>Song, Chunjiao</creator><creator>Yuan, Chengliang</creator><general>Springer Berlin Heidelberg</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>7S9</scope><scope>L.6</scope></search><sort><creationdate>20240501</creationdate><title>lncRNA MIAT promotes luminal B breast cancer cell proliferation, migration, and invasion in vitro</title><author>Mi, Jintao ; Zhang, Hongsheng ; Jiang, Xuemei ; Yi, Ying ; Cao, Weiwei ; Song, Chunjiao ; Yuan, Chengliang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-978fdff14418a52a6332b6ae7fd7ffcef85a204de52962574abfbe8265e960ff3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animal Genetics and Genomics</topic><topic>Apoptosis</topic><topic>bioinformatics</topic><topic>Biomedical and Life Sciences</topic><topic>Breast cancer</topic><topic>breast neoplasms</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell death</topic><topic>Cell migration</topic><topic>Cell Movement - genetics</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Human Genetics</topic><topic>Human Genetics • Original Paper</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>ligands</topic><topic>Microbial Genetics and Genomics</topic><topic>MicroRNAs - genetics</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - genetics</topic><topic>neoplasm cells</topic><topic>Non-coding RNA</topic><topic>oncogenes</topic><topic>Plant Genetics and Genomics</topic><topic>programmed cell death</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mi, Jintao</creatorcontrib><creatorcontrib>Zhang, Hongsheng</creatorcontrib><creatorcontrib>Jiang, Xuemei</creatorcontrib><creatorcontrib>Yi, Ying</creatorcontrib><creatorcontrib>Cao, Weiwei</creatorcontrib><creatorcontrib>Song, Chunjiao</creatorcontrib><creatorcontrib>Yuan, Chengliang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Journal of applied genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mi, Jintao</au><au>Zhang, Hongsheng</au><au>Jiang, Xuemei</au><au>Yi, Ying</au><au>Cao, Weiwei</au><au>Song, Chunjiao</au><au>Yuan, Chengliang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>lncRNA MIAT promotes luminal B breast cancer cell proliferation, migration, and invasion in vitro</atitle><jtitle>Journal of applied genetics</jtitle><stitle>J Appl Genetics</stitle><addtitle>J Appl Genet</addtitle><date>2024-05-01</date><risdate>2024</risdate><volume>65</volume><issue>2</issue><spage>309</spage><epage>319</epage><pages>309-319</pages><issn>1234-1983</issn><eissn>2190-3883</eissn><abstract>Long noncoding RNAs (lncRNAs) play a role in the emergence and progression of several human tumors, including luminal B breast cancer (BC). The biological functions and potential mechanisms of lncRNA myocardial infarction-associated transcripts (MIAT) in luminal B BC, on the contrary, are unknown. In this work, we used UALCAN database analysis to find high expression of lncRNA MIAT in luminal BC tissues and also confirmed high levels of lncRNA MIAT expression in luminal B BC tissues and cells. In vitro knockdown of MIAT inhibited the proliferation, migration, and invasion of BT474 cells. In addition, we found that miR-150-5p levels were significantly reduced in luminal B BC specimens and cells, and miR-150-5p levels were significantly increased when MIAT was knocked down. And TIMER database analysis showed that MIAT was positively associated with PDL1. Through bioinformatic tools and in vitro experiments, lncRNA MIAT could function as a competitive endogenous RNA (CeRNA) to further regulate programmed cell death ligand 1 (PDL1) expression by directly sponging miR-150-5p. In conclusion, our data suggest that MIAT, an oncogene, may sponge miR-150-5p to regulate PDL1 expression and affect proliferation, migration, and invasion in luminal B BC in vitro.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>37987972</pmid><doi>10.1007/s13353-023-00807-2</doi><tpages>11</tpages></addata></record> |
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subjects | Animal Genetics and Genomics Apoptosis bioinformatics Biomedical and Life Sciences Breast cancer breast neoplasms Breast Neoplasms - genetics Breast Neoplasms - pathology Cell death Cell migration Cell Movement - genetics Cell proliferation Cell Proliferation - genetics Female Gene Expression Regulation, Neoplastic Human Genetics Human Genetics • Original Paper Humans Life Sciences ligands Microbial Genetics and Genomics MicroRNAs - genetics Myocardial infarction Myocardial Infarction - genetics neoplasm cells Non-coding RNA oncogenes Plant Genetics and Genomics programmed cell death RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism |
title | lncRNA MIAT promotes luminal B breast cancer cell proliferation, migration, and invasion in vitro |
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