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dc.contributor.authorKe, Hao
dc.contributor.authorZhao, Limin
dc.contributor.authorFeng, Xu
dc.contributor.authorXu, Haibo
dc.contributor.authorZou, Li
dc.contributor.authorYang, Qin
dc.contributor.authorSu, Xiaosan
dc.contributor.authorPeng, Lingtao
dc.contributor.authorJiao, Baowei
dc.date2022-08-11T08:09:45.000
dc.date.accessioned2022-08-23T16:42:28Z
dc.date.available2022-08-23T16:42:28Z
dc.date.issued2016-04-27
dc.date.submitted2016-11-30
dc.identifier.citationGene Regul Syst Bio. 2016 Apr 27;10(Suppl 1):11-7. doi: 10.4137/GRSB.S29414. eCollection 2016. <a href="http://dx.doi.org/10.4137/GRSB.S29414">Link to article on publisher's site</a>
dc.identifier.issn1177-6250 (Linking)
dc.identifier.doi10.4137/GRSB.S29414
dc.identifier.pmid27147820
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40099
dc.description.abstractIncreasing evidence shows that long noncoding RNAs (lncRNAs) have important roles in the regulation of multiple cellular processes, including cell division, cell growth, and apoptosis, as well as cancer metastasis and neurological disease progression; however, the mechanism of how lncRNAs regulate these processes is not well established. In this study, we demonstrated that downregulating the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in breast cancer cells inhibited cell growth and induced cell apoptosis. In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis. These results indicate a novel interaction between NEAT1, miR-548ar-3p, and FUS and their role in the regulation of breast cancer cell apoptosis.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27147820&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsCopyright the authors, publisher and licensee Libertas Academica Limited.
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/
dc.subjectFUS
dc.subjectNEAT1
dc.subjectcell apoptosis
dc.subjectlncRNA
dc.subjectmiR-548ar-3p
dc.subjectCancer Biology
dc.subjectCell Biology
dc.titleNEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548
dc.typeJournal Article
dc.source.journaltitleGene regulation and systems biology
dc.source.volume10
dc.source.issueSuppl 1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3905&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2900
dc.identifier.contextkey9425538
refterms.dateFOA2022-08-23T16:42:28Z
html.description.abstract<p>Increasing evidence shows that long noncoding RNAs (lncRNAs) have important roles in the regulation of multiple cellular processes, including cell division, cell growth, and apoptosis, as well as cancer metastasis and neurological disease progression; however, the mechanism of how lncRNAs regulate these processes is not well established. In this study, we demonstrated that downregulating the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in breast cancer cells inhibited cell growth and induced cell apoptosis. In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis. These results indicate a novel interaction between NEAT1, miR-548ar-3p, and FUS and their role in the regulation of breast cancer cell apoptosis.</p>
dc.identifier.submissionpathoapubs/2900
dc.contributor.departmentRNA Therapeutics Institute
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology
dc.source.pages11-7


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Copyright the authors, publisher and licensee Libertas Academica Limited.
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