BACKGROUND： The majority of mammalian genomes have been found to be transcribed into non-coding RNAs. One category of non-coding RNAs is classified as long non-coding RNAs （lncRNAs） based on their transcript sizes ...BACKGROUND： The majority of mammalian genomes have been found to be transcribed into non-coding RNAs. One category of non-coding RNAs is classified as long non-coding RNAs （lncRNAs） based on their transcript sizes larger than 200 nucleotides. Growing evidence has shown that lncRNAs are not junk transcripts and play regulatory roles in multiple aspects of biological processes. Dysregulation of lncRNA expression has also been linked to diseases, in particular cancer. Therefore, studies of lncRNAs have attracted significant interest in the field of medical research. Nuclear enriched abundant transcript 1 （NEAT1）, a nuclear lncRNA, has recently emerged as a key regulator involved in various cellular processes, physiological responses, developmental processes, and disease development and progression. OBJECTIVE： This review will summarize and discuss the most recent findings with regard to the roles of NEAT1 in the function of the nuclear paraspeckle, cellular pathways, and physiological responses and processes. Particularly, the most recently reported studies regarding the pathological roles of deregulated NEAT1 in cancer are highlighted in this review. METHODS： We performed a systematic literature search using the Pubmed search engine. Studies published over the past 8 years （between January 2009 and August 2016） were the sources of literature review. The following keywords were used： ＂Nuclear enriched abundant transcript 1,＂ ＂NEATI,＂ and ＂paraspeckles.＂ RESULTS： The Pubmed search identified 34 articles related to the topic of the review. Among the identified literature, 13 articles report findings related to cellular functions of NEAT1 and eight articles are the investigations of physiological functions of NEAT1. The remaining 13 articles are studies of the roles of NEAT1 in cancers. CONCLUSION： Recent advances in NEAT1 studies reveal the multifimctional roles of NEAT1 in various biological processes, which are beyond its role in nuclear paraspeckles. Recent studies also indicate 展开更多
This study aimed to assess the role of microRNAs(miRNAs)in regulating monocarboxylate transporter-1(MCT1)expression in rat brain after permanent focal cerebral ischemia to identify a new target for early treatment of ...This study aimed to assess the role of microRNAs(miRNAs)in regulating monocarboxylate transporter-1(MCT1)expression in rat brain after permanent focal cerebral ischemia to identify a new target for early treatment of cerebral ischemia.Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion(pMCAO)in rats.Morphology and protein expression levels of MCT1 were assessed by immunofluorescence and Western blotting.Using bioinformatics and double luciferase reporter assays,rno-miR-124-3p was selected as a direct target for rat MCT1.Expression of rno-miR-124-3p after pMCAO was detected.Then,rats were treated with rno-miR-124-3p agomir via lateral ventricle injection,and after 6 h or 24 h ischemia,rno-miR-124-3p expression and gene and protein expression of MCT-1 were detected by qRT-PCR and Western blotting.Brain infarction was identified by 2,3,5-triphenyltetrazolium chloride(TTC)staining.Results showed that pMCAO induced brain infarction and increased the expression of MCT1.The levels of rno-miR-124-3p after pMCAO were in contrast to those of MCT1 protein in ischemic region,while declined after 3,6 and 12 h of pMCAO in ischemic penumbra.After administration of rno-miR-124-3p agomir,MCT1 mRNA and protein levels were increased after 6 h of pMCAO,while decreased after 24 h of pMCAO.Meanwhile,rno-miR-124-3p levels increased after both times.TTC staining showed treatment with rno-miR-124-3p agomir reduced brain infarction.The role of rno-miR-124-3p in regulating MCT1 was as a positive regulator after 6 h of pMCAO,while a negative regulator after 24 h of pMCAO,however,both activities had protective effects against cerebral ischemia.展开更多
文摘BACKGROUND： The majority of mammalian genomes have been found to be transcribed into non-coding RNAs. One category of non-coding RNAs is classified as long non-coding RNAs （lncRNAs） based on their transcript sizes larger than 200 nucleotides. Growing evidence has shown that lncRNAs are not junk transcripts and play regulatory roles in multiple aspects of biological processes. Dysregulation of lncRNA expression has also been linked to diseases, in particular cancer. Therefore, studies of lncRNAs have attracted significant interest in the field of medical research. Nuclear enriched abundant transcript 1 （NEAT1）, a nuclear lncRNA, has recently emerged as a key regulator involved in various cellular processes, physiological responses, developmental processes, and disease development and progression. OBJECTIVE： This review will summarize and discuss the most recent findings with regard to the roles of NEAT1 in the function of the nuclear paraspeckle, cellular pathways, and physiological responses and processes. Particularly, the most recently reported studies regarding the pathological roles of deregulated NEAT1 in cancer are highlighted in this review. METHODS： We performed a systematic literature search using the Pubmed search engine. Studies published over the past 8 years （between January 2009 and August 2016） were the sources of literature review. The following keywords were used： ＂Nuclear enriched abundant transcript 1,＂ ＂NEATI,＂ and ＂paraspeckles.＂ RESULTS： The Pubmed search identified 34 articles related to the topic of the review. Among the identified literature, 13 articles report findings related to cellular functions of NEAT1 and eight articles are the investigations of physiological functions of NEAT1. The remaining 13 articles are studies of the roles of NEAT1 in cancers. CONCLUSION： Recent advances in NEAT1 studies reveal the multifimctional roles of NEAT1 in various biological processes, which are beyond its role in nuclear paraspeckles. Recent studies also indicate
文摘This study aimed to assess the role of microRNAs(miRNAs)in regulating monocarboxylate transporter-1(MCT1)expression in rat brain after permanent focal cerebral ischemia to identify a new target for early treatment of cerebral ischemia.Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion(pMCAO)in rats.Morphology and protein expression levels of MCT1 were assessed by immunofluorescence and Western blotting.Using bioinformatics and double luciferase reporter assays,rno-miR-124-3p was selected as a direct target for rat MCT1.Expression of rno-miR-124-3p after pMCAO was detected.Then,rats were treated with rno-miR-124-3p agomir via lateral ventricle injection,and after 6 h or 24 h ischemia,rno-miR-124-3p expression and gene and protein expression of MCT-1 were detected by qRT-PCR and Western blotting.Brain infarction was identified by 2,3,5-triphenyltetrazolium chloride(TTC)staining.Results showed that pMCAO induced brain infarction and increased the expression of MCT1.The levels of rno-miR-124-3p after pMCAO were in contrast to those of MCT1 protein in ischemic region,while declined after 3,6 and 12 h of pMCAO in ischemic penumbra.After administration of rno-miR-124-3p agomir,MCT1 mRNA and protein levels were increased after 6 h of pMCAO,while decreased after 24 h of pMCAO.Meanwhile,rno-miR-124-3p levels increased after both times.TTC staining showed treatment with rno-miR-124-3p agomir reduced brain infarction.The role of rno-miR-124-3p in regulating MCT1 was as a positive regulator after 6 h of pMCAO,while a negative regulator after 24 h of pMCAO,however,both activities had protective effects against cerebral ischemia.
