New Insights into Long Non-Coding RNA MALAT1 in Cancer and Metastasis
Metastasis-associated lung adenocarcinoma transcript 1 ( ) is one of the most abundant, long non-coding RNAs (lncRNAs) in normal tissues. This lncRNA is highly conserved among mammalian species, and based on in vitro results, has been reported to regulate alternative pre-mRNA splicing and gene expre...
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description | Metastasis-associated lung adenocarcinoma transcript 1 (
) is one of the most abundant, long non-coding RNAs (lncRNAs) in normal tissues. This lncRNA is highly conserved among mammalian species, and based on in vitro results, has been reported to regulate alternative pre-mRNA splicing and gene expression. However,
knockout mice develop and grow normally, and do not show alterations in alternative splicing. While
was originally described as a prognostic marker of lung cancer metastasis, emerging evidence has linked this lncRNA to other cancers, such as breast cancer, prostate cancer, pancreatic cancer, glioma, and leukemia. The role described for
is dependent on the cancer types and the experimental model systems. Notably, different or opposite phenotypes resulting from different strategies for inactivating
have been observed, which led to distinct models for
s functions and mechanisms of action in cancer and metastasis. In this review, we reflect on different experimental strategies used to study
s functions, and discuss the current mechanistic models of this highly abundant and conserved lncRNA. |
doi_str_mv | 10.3390/cancers11020216 |
format | Article |
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) is one of the most abundant, long non-coding RNAs (lncRNAs) in normal tissues. This lncRNA is highly conserved among mammalian species, and based on in vitro results, has been reported to regulate alternative pre-mRNA splicing and gene expression. However,
knockout mice develop and grow normally, and do not show alterations in alternative splicing. While
was originally described as a prognostic marker of lung cancer metastasis, emerging evidence has linked this lncRNA to other cancers, such as breast cancer, prostate cancer, pancreatic cancer, glioma, and leukemia. The role described for
is dependent on the cancer types and the experimental model systems. Notably, different or opposite phenotypes resulting from different strategies for inactivating
have been observed, which led to distinct models for
s functions and mechanisms of action in cancer and metastasis. In this review, we reflect on different experimental strategies used to study
s functions, and discuss the current mechanistic models of this highly abundant and conserved lncRNA.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers11020216</identifier><identifier>PMID: 30781877</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adenocarcinoma ; Alternative splicing ; Binding sites ; Breast cancer ; Cell growth ; CRISPR ; Gene expression ; Genetic engineering ; Glioma ; Lung cancer ; Metastases ; Metastasis ; Non-coding RNA ; Pancreatic cancer ; Phenotypes ; Prostate cancer ; Review ; Transcription ; Tumors</subject><ispartof>Cancers, 2019-02, Vol.11 (2), p.216</ispartof><rights>2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 by the authors. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-e7437686bdbe5ff17b953d073bbce625975a9f86d10c4ae06e5a7fc64d42e73a3</citedby><cites>FETCH-LOGICAL-c421t-e7437686bdbe5ff17b953d073bbce625975a9f86d10c4ae06e5a7fc64d42e73a3</cites><orcidid>0000-0001-9965-989X</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/PMC6406606/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406606/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30781877$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Yutong</creatorcontrib><creatorcontrib>Ma, Li</creatorcontrib><title>New Insights into Long Non-Coding RNA MALAT1 in Cancer and Metastasis</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>Metastasis-associated lung adenocarcinoma transcript 1 (
) is one of the most abundant, long non-coding RNAs (lncRNAs) in normal tissues. This lncRNA is highly conserved among mammalian species, and based on in vitro results, has been reported to regulate alternative pre-mRNA splicing and gene expression. However,
knockout mice develop and grow normally, and do not show alterations in alternative splicing. While
was originally described as a prognostic marker of lung cancer metastasis, emerging evidence has linked this lncRNA to other cancers, such as breast cancer, prostate cancer, pancreatic cancer, glioma, and leukemia. The role described for
is dependent on the cancer types and the experimental model systems. Notably, different or opposite phenotypes resulting from different strategies for inactivating
have been observed, which led to distinct models for
s functions and mechanisms of action in cancer and metastasis. In this review, we reflect on different experimental strategies used to study
s functions, and discuss the current mechanistic models of this highly abundant and conserved lncRNA.</description><subject>Adenocarcinoma</subject><subject>Alternative splicing</subject><subject>Binding sites</subject><subject>Breast cancer</subject><subject>Cell growth</subject><subject>CRISPR</subject><subject>Gene expression</subject><subject>Genetic engineering</subject><subject>Glioma</subject><subject>Lung cancer</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Non-coding RNA</subject><subject>Pancreatic cancer</subject><subject>Phenotypes</subject><subject>Prostate cancer</subject><subject>Review</subject><subject>Transcription</subject><subject>Tumors</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkd1LwzAUxYMobsw9-yYFX3ypy1eT9kUoY-qgmyDzOaRpunV0yWxaxf_e6OaYuwTugfvLSS4HgGsE7wlJ4EhJo3TjEIIYYsTOQB9DjkPGEnp-pHtg6Nwa-iIEccYvQY9AHqOY8z6YzPVnMDWuWq5aF1SmtUFmzTKYWxOObVF5-TpPg1mapQvk58H499FAmiKY6VY6fyp3BS5KWTs93PcBeHucLMbPYfbyNB2nWagoRm2oOSWcxSwvch2VJeJ5EpECcpLnSjMcJTySSRmzAkFFpYZMR5KXitGCYs2JJAPwsPPddvlGF0qbtpG12DbVRjZfwspK_J-YaiWW9kMwChmDzBvc7Q0a-95p14pN5ZSua2m07ZzAKKaIwgQRj96eoGvbNcavJ3BEeQRxEseeGu0o1VjnGl0ePoOg-ElJnKTkb9wc73Dg_zIh35ymjQg</recordid><startdate>20190213</startdate><enddate>20190213</enddate><creator>Sun, Yutong</creator><creator>Ma, Li</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</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>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9965-989X</orcidid></search><sort><creationdate>20190213</creationdate><title>New Insights into Long Non-Coding RNA MALAT1 in Cancer and Metastasis</title><author>Sun, Yutong ; Ma, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-e7437686bdbe5ff17b953d073bbce625975a9f86d10c4ae06e5a7fc64d42e73a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenocarcinoma</topic><topic>Alternative splicing</topic><topic>Binding sites</topic><topic>Breast cancer</topic><topic>Cell growth</topic><topic>CRISPR</topic><topic>Gene expression</topic><topic>Genetic engineering</topic><topic>Glioma</topic><topic>Lung cancer</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Non-coding RNA</topic><topic>Pancreatic cancer</topic><topic>Phenotypes</topic><topic>Prostate cancer</topic><topic>Review</topic><topic>Transcription</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Yutong</creatorcontrib><creatorcontrib>Ma, Li</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</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>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Yutong</au><au>Ma, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>New Insights into Long Non-Coding RNA MALAT1 in Cancer and Metastasis</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2019-02-13</date><risdate>2019</risdate><volume>11</volume><issue>2</issue><spage>216</spage><pages>216-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Metastasis-associated lung adenocarcinoma transcript 1 (
) is one of the most abundant, long non-coding RNAs (lncRNAs) in normal tissues. This lncRNA is highly conserved among mammalian species, and based on in vitro results, has been reported to regulate alternative pre-mRNA splicing and gene expression. However,
knockout mice develop and grow normally, and do not show alterations in alternative splicing. While
was originally described as a prognostic marker of lung cancer metastasis, emerging evidence has linked this lncRNA to other cancers, such as breast cancer, prostate cancer, pancreatic cancer, glioma, and leukemia. The role described for
is dependent on the cancer types and the experimental model systems. Notably, different or opposite phenotypes resulting from different strategies for inactivating
have been observed, which led to distinct models for
s functions and mechanisms of action in cancer and metastasis. In this review, we reflect on different experimental strategies used to study
s functions, and discuss the current mechanistic models of this highly abundant and conserved lncRNA.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>30781877</pmid><doi>10.3390/cancers11020216</doi><orcidid>https://orcid.org/0000-0001-9965-989X</orcidid><oa>free_for_read</oa></addata></record> |
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source | MDPI - Multidisciplinary Digital Publishing Institute; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
subjects | Adenocarcinoma Alternative splicing Binding sites Breast cancer Cell growth CRISPR Gene expression Genetic engineering Glioma Lung cancer Metastases Metastasis Non-coding RNA Pancreatic cancer Phenotypes Prostate cancer Review Transcription Tumors |
title | New Insights into Long Non-Coding RNA MALAT1 in Cancer and Metastasis |
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