Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1
Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) is a long noncoding RNA whose transcript is around 8 kb in length. As an important stress response molecule, MALAT1 can be expressed differently under stress conditions, such as hypoxia, high glucose, hydrogen peroxide, ultraviolet irra...
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| Veröffentlicht in: | Journal of cellular physiology 2019-01, Vol.234 (1), p.134-151 |
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| description | Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) is a long noncoding RNA whose transcript is around 8 kb in length. As an important stress response molecule, MALAT1 can be expressed differently under stress conditions, such as hypoxia, high glucose, hydrogen peroxide, ultraviolet irradiation, infection, and chemical stimulation. MALAT1 is involved in regulating multiple cell behaviors, such as proliferation, apoptosis, differentiation, migration, epithelial–mesenchymal transition, autophagy, and morphological maintenance. Extensive evidence show that MALAT1 plays critical roles in the physiopathological process of embryo implantation, angiogenesis, tissue inflammation, tumor progression, liver fibrosis, cardiovascular remodeling, and diabetes progression by regulating gene transcription, forming RNA–protein complexes with proteins as a structural component, regulating protein activity, assisting protein localization, mediating epigenetic changes, or by acting as a competing endogenous RNA. Furthermore, MALAT1 can affect the sensitivity of chemotherapy and radiotherapy; therefore, it could be used as a potential drug target for chemotherapy and radiotherapy sensitization. The levels of MALAT1 are reported to be overexpressed in most tumor tissues or sera, and the expression levels of MALAT1 often affect the tumor size, stage, lymph node metastasis, and distant invasion. Therefore, MALAT1 can be used as a biomarker for early diagnosis, severity assessment, or prognostic assessment. This review outlines the current understanding of the biological role and function of MALAT1. In the meantime, we have summarized the mechanisms involved in the reulation of MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.
This review outlines the current understanding of the biological roles and functions of lncRNA MALAT1. In the meantime, this review summarizes the mechanisms involved in regulating MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes. |
| doi_str_mv | 10.1002/jcp.26759 |
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This review outlines the current understanding of the biological roles and functions of lncRNA MALAT1. In the meantime, this review summarizes the mechanisms involved in regulating MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.26759</identifier><identifier>PMID: 30132842</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Adenocarcinoma ; Angiogenesis ; Apoptosis ; Apoptosis - genetics ; Autophagy ; biomarker ; Biomarkers ; Biomarkers, Tumor - genetics ; Cell Proliferation - genetics ; Chemotherapy ; competing endogenous RNA ; Diabetes mellitus ; Embryos ; Epigenetics ; Epithelial-Mesenchymal Transition - genetics ; Fibrosis ; Gene Expression Regulation, Neoplastic - genetics ; Humans ; Hydrogen peroxide ; Hypoxia ; Implantation ; Irradiation ; Liver ; Localization ; Lung cancer ; Lungs ; Lymph nodes ; MALAT1 ; Mesenchyme ; Metastases ; Metastasis ; Organic chemistry ; Phagocytosis ; Proteins ; Radiation therapy ; Regulatory mechanisms (biology) ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; Signal Transduction - genetics ; signaling pathway ; stress response ; Stress, Physiological - genetics ; Transcription ; Tumors ; Ultraviolet radiation</subject><ispartof>Journal of cellular physiology, 2019-01, Vol.234 (1), p.134-151</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3889-f37b3d72137599d7b457e8b795c6980b69050eecc6afa04dae0773020ba123433</citedby><cites>FETCH-LOGICAL-c3889-f37b3d72137599d7b457e8b795c6980b69050eecc6afa04dae0773020ba123433</cites><orcidid>0000-0002-6747-1486</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.26759$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.26759$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27928,27929,45578,45579</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30132842$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lei, Li</creatorcontrib><creatorcontrib>Chen, Jing</creatorcontrib><creatorcontrib>Huang, Jinhua</creatorcontrib><creatorcontrib>Lu, Jianyun</creatorcontrib><creatorcontrib>Pei, Shiyao</creatorcontrib><creatorcontrib>Ding, Shu</creatorcontrib><creatorcontrib>Kang, Liyang</creatorcontrib><creatorcontrib>Xiao, Rong</creatorcontrib><creatorcontrib>Zeng, Qinghai</creatorcontrib><title>Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) is a long noncoding RNA whose transcript is around 8 kb in length. As an important stress response molecule, MALAT1 can be expressed differently under stress conditions, such as hypoxia, high glucose, hydrogen peroxide, ultraviolet irradiation, infection, and chemical stimulation. MALAT1 is involved in regulating multiple cell behaviors, such as proliferation, apoptosis, differentiation, migration, epithelial–mesenchymal transition, autophagy, and morphological maintenance. Extensive evidence show that MALAT1 plays critical roles in the physiopathological process of embryo implantation, angiogenesis, tissue inflammation, tumor progression, liver fibrosis, cardiovascular remodeling, and diabetes progression by regulating gene transcription, forming RNA–protein complexes with proteins as a structural component, regulating protein activity, assisting protein localization, mediating epigenetic changes, or by acting as a competing endogenous RNA. Furthermore, MALAT1 can affect the sensitivity of chemotherapy and radiotherapy; therefore, it could be used as a potential drug target for chemotherapy and radiotherapy sensitization. The levels of MALAT1 are reported to be overexpressed in most tumor tissues or sera, and the expression levels of MALAT1 often affect the tumor size, stage, lymph node metastasis, and distant invasion. Therefore, MALAT1 can be used as a biomarker for early diagnosis, severity assessment, or prognostic assessment. This review outlines the current understanding of the biological role and function of MALAT1. In the meantime, we have summarized the mechanisms involved in the reulation of MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.
This review outlines the current understanding of the biological roles and functions of lncRNA MALAT1. In the meantime, this review summarizes the mechanisms involved in regulating MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.</description><subject>Adenocarcinoma</subject><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Autophagy</subject><subject>biomarker</subject><subject>Biomarkers</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Chemotherapy</subject><subject>competing endogenous RNA</subject><subject>Diabetes mellitus</subject><subject>Embryos</subject><subject>Epigenetics</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Fibrosis</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Humans</subject><subject>Hydrogen peroxide</subject><subject>Hypoxia</subject><subject>Implantation</subject><subject>Irradiation</subject><subject>Liver</subject><subject>Localization</subject><subject>Lung cancer</subject><subject>Lungs</subject><subject>Lymph nodes</subject><subject>MALAT1</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Organic chemistry</subject><subject>Phagocytosis</subject><subject>Proteins</subject><subject>Radiation therapy</subject><subject>Regulatory mechanisms (biology)</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Signal Transduction - genetics</subject><subject>signaling pathway</subject><subject>stress response</subject><subject>Stress, Physiological - genetics</subject><subject>Transcription</subject><subject>Tumors</subject><subject>Ultraviolet radiation</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM9O3DAQh60KVBbaQ18AReJSDoGxHcfxsVqVf0KCAz1bE8ehXiX21k6E9sYj8Iw8CW6XckBCsjSy5tNvZj5CvlE4oQDsdGXWJ6yWQn0iCwpKllUt2A5Z5B4tlajoHtlPaQUASnH-mexxoJw1FVsQfTZ7M7ngU4G-K6K9nwecQtwUozW_0bs0piL0-Tdhys-l58cnTCkYh5PtimH29wV21geD0TgfRiymiD6Z6NZTQb-Q3R6HZL--1gPy6-zn3fKivL45v1z-uC4NbxpV9ly2vJOM8nyF6mRbCWmbViphatVAWysQYK0xNfYIVYcWpOTAoEXKeMX5Afm-zV3H8Ge2adKjS8YOA3ob5qQZKNpQUdVVRo_eoaswR5-303m-EEqKWmbqeEuZGFKKttfr6EaMG01B_7Wus3X9z3pmD18T53a03Rv5X3MGTrfAgxvs5uMkfbW83Ua-AF2BjLY</recordid><startdate>201901</startdate><enddate>201901</enddate><creator>Lei, Li</creator><creator>Chen, Jing</creator><creator>Huang, Jinhua</creator><creator>Lu, Jianyun</creator><creator>Pei, Shiyao</creator><creator>Ding, Shu</creator><creator>Kang, Liyang</creator><creator>Xiao, Rong</creator><creator>Zeng, Qinghai</creator><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6747-1486</orcidid></search><sort><creationdate>201901</creationdate><title>Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1</title><author>Lei, Li ; Chen, Jing ; Huang, Jinhua ; Lu, Jianyun ; Pei, Shiyao ; Ding, Shu ; Kang, Liyang ; Xiao, Rong ; Zeng, Qinghai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3889-f37b3d72137599d7b457e8b795c6980b69050eecc6afa04dae0773020ba123433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenocarcinoma</topic><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Autophagy</topic><topic>biomarker</topic><topic>Biomarkers</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Chemotherapy</topic><topic>competing endogenous RNA</topic><topic>Diabetes mellitus</topic><topic>Embryos</topic><topic>Epigenetics</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Fibrosis</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Humans</topic><topic>Hydrogen peroxide</topic><topic>Hypoxia</topic><topic>Implantation</topic><topic>Irradiation</topic><topic>Liver</topic><topic>Localization</topic><topic>Lung cancer</topic><topic>Lungs</topic><topic>Lymph nodes</topic><topic>MALAT1</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Organic chemistry</topic><topic>Phagocytosis</topic><topic>Proteins</topic><topic>Radiation therapy</topic><topic>Regulatory mechanisms (biology)</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>Signal Transduction - genetics</topic><topic>signaling pathway</topic><topic>stress response</topic><topic>Stress, Physiological - genetics</topic><topic>Transcription</topic><topic>Tumors</topic><topic>Ultraviolet radiation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lei, Li</creatorcontrib><creatorcontrib>Chen, Jing</creatorcontrib><creatorcontrib>Huang, Jinhua</creatorcontrib><creatorcontrib>Lu, Jianyun</creatorcontrib><creatorcontrib>Pei, Shiyao</creatorcontrib><creatorcontrib>Ding, Shu</creatorcontrib><creatorcontrib>Kang, Liyang</creatorcontrib><creatorcontrib>Xiao, Rong</creatorcontrib><creatorcontrib>Zeng, Qinghai</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lei, Li</au><au>Chen, Jing</au><au>Huang, Jinhua</au><au>Lu, Jianyun</au><au>Pei, Shiyao</au><au>Ding, Shu</au><au>Kang, Liyang</au><au>Xiao, Rong</au><au>Zeng, Qinghai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2019-01</date><risdate>2019</risdate><volume>234</volume><issue>1</issue><spage>134</spage><epage>151</epage><pages>134-151</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) is a long noncoding RNA whose transcript is around 8 kb in length. As an important stress response molecule, MALAT1 can be expressed differently under stress conditions, such as hypoxia, high glucose, hydrogen peroxide, ultraviolet irradiation, infection, and chemical stimulation. MALAT1 is involved in regulating multiple cell behaviors, such as proliferation, apoptosis, differentiation, migration, epithelial–mesenchymal transition, autophagy, and morphological maintenance. Extensive evidence show that MALAT1 plays critical roles in the physiopathological process of embryo implantation, angiogenesis, tissue inflammation, tumor progression, liver fibrosis, cardiovascular remodeling, and diabetes progression by regulating gene transcription, forming RNA–protein complexes with proteins as a structural component, regulating protein activity, assisting protein localization, mediating epigenetic changes, or by acting as a competing endogenous RNA. Furthermore, MALAT1 can affect the sensitivity of chemotherapy and radiotherapy; therefore, it could be used as a potential drug target for chemotherapy and radiotherapy sensitization. The levels of MALAT1 are reported to be overexpressed in most tumor tissues or sera, and the expression levels of MALAT1 often affect the tumor size, stage, lymph node metastasis, and distant invasion. Therefore, MALAT1 can be used as a biomarker for early diagnosis, severity assessment, or prognostic assessment. This review outlines the current understanding of the biological role and function of MALAT1. In the meantime, we have summarized the mechanisms involved in the reulation of MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.
This review outlines the current understanding of the biological roles and functions of lncRNA MALAT1. In the meantime, this review summarizes the mechanisms involved in regulating MALAT1 expression and the mechanisms by which MALAT1 regulates the physiological and pathological processes.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30132842</pmid><doi>10.1002/jcp.26759</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0002-6747-1486</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma Angiogenesis Apoptosis Apoptosis - genetics Autophagy biomarker Biomarkers Biomarkers, Tumor - genetics Cell Proliferation - genetics Chemotherapy competing endogenous RNA Diabetes mellitus Embryos Epigenetics Epithelial-Mesenchymal Transition - genetics Fibrosis Gene Expression Regulation, Neoplastic - genetics Humans Hydrogen peroxide Hypoxia Implantation Irradiation Liver Localization Lung cancer Lungs Lymph nodes MALAT1 Mesenchyme Metastases Metastasis Organic chemistry Phagocytosis Proteins Radiation therapy Regulatory mechanisms (biology) Ribonucleic acid RNA RNA, Long Noncoding - genetics Signal Transduction - genetics signaling pathway stress response Stress, Physiological - genetics Transcription Tumors Ultraviolet radiation |
| title | Functions and regulatory mechanisms of metastasis‐associated lung adenocarcinoma transcript 1 |
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