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TGF-β2-induced NEAT1 regulates lens epithelial cell proliferation,migration and EMT by the miR-26a-5p/FANCE axis 被引量:2
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作者 Xiao-Hui Yu Shao-Yi Liu Cheng-Fang Li 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2021年第11期1674-1682,共9页
AIM:To explore the regulatory mechanism of nuclear paraspeckle assembly transcript 1(NEAT1)in the pathogenesis of posterior capsule opacification(PCO).METHODS:Quantitative reverse transcription polymerase chain reacti... AIM:To explore the regulatory mechanism of nuclear paraspeckle assembly transcript 1(NEAT1)in the pathogenesis of posterior capsule opacification(PCO).METHODS:Quantitative reverse transcription polymerase chain reaction(RT-q PCR)was executed to analyze NEAT1 and micro RNA(miR)-26a-5p expression in transforming growth factor-beta 2(TGF-β2)-disposed lens epithelial cells(LECs).The proliferation,cell cycle progression,apoptosis,and migration of TGF-β2-disposed LECs were evaluated.The relationship between NEAT1 or fanconi anemia(FA)complementation group E(FANCE)and miR-26a-5p was verified by dual-luciferase reporter assay.RESULTS:TGF-β2 induced NEAT1 expression in LECs.NEAT1 inhibition accelerated apoptosis,cell cycle arrest,decreased proliferation,epithelial-mesenchymal transition(EMT),and migration of TGF-β2-disposed LECs.NEAT1 sponged miR-26a-5p to further regulate FANCE expression.Rescue experiments presented that miR-26a-5p downregulation overturned NEAT1 silencing-mediated impacts on TGF-β2-disposed LEC biological behaviors.Additionally,FANCE overexpression reversed miR-26a-5p mimic-mediated impacts on TGF-β2-disposed LEC biological behaviors.CONCLUSION:TGF-β2-induced NEAT1 facilitates LEC proliferation,migration,and EMT by upregulating FANCE via sequestering miR-26a-5p. 展开更多
关键词 posterior capsule opacification transforming growth factor-beta 2 nuclear paraspeckle assembly transcript 1 miRNA-26a-5p fanconi anemia complementation group e
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FOXO1-miR-506 axis promotes chemosensitivity to temozolomide and suppresses invasiveness in glioblastoma through a feedback loop of FOXO1/miR-506/ETS1/FOXO1
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作者 Chao CHEN Yu’e LIU +3 位作者 Hongxiang WANG Xu ZHANG Yufeng SHI Juxiang CHEN 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2023年第8期698-710,共13页
To explore the role of forkhead box protein O1(FOXO1)in the progression of glioblastoma multiforme(GBM)and related drug resistance,we deciphered the roles of FOXO1 and miR-506 in proliferation,apoptosis,migration,inva... To explore the role of forkhead box protein O1(FOXO1)in the progression of glioblastoma multiforme(GBM)and related drug resistance,we deciphered the roles of FOXO1 and miR-506 in proliferation,apoptosis,migration,invasion,autophagy,and temozolomide(TMZ)sensitivity in the U251 cell line using in vitro and in vivo experiments.Cell viability was tested by a cell counting kit-8(CCK8)kit;migration and invasion were checked by the scratching assay;apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL)staining and flow cytometry.The construction of plasmids and dual-luciferase reporter experiment were carried out to find the interaction site between FOXO1 and miR-506.Immunohistochemistry was done to check the protein level in tumors after the in vivo experiment.We found that the FOXO1-miR-506 axis suppresses GBM cell invasion and migration and promotes GBM chemosensitivity to TMZ,which was mediated by autophagy.FOXO1 upregulates miR-506 by binding to its promoter to enhance transcriptional activation.MiR-506 could downregulate E26 transformation-specific 1(ETS1)expression by targeting its 3'-untranslated region(UTR).Interestingly,ETS1 promoted FOXO1 translocation from the nucleus to the cytosol and further suppressed the FOXO1-miR-506 axis in GBM cells.Consistently,both miR-506 inhibition and ETS1 overexpression could rescue FOXO1 overactivation-mediated TMZ chemosensitivity in mouse models.Our study demonstrated a negative feedback loop of FOXO1/miR-506/ETS1/FOXO1 in GBM in regulating invasiveness and chemosensitivity.Thus,the above axis might be a promising therapeutic target for GBM. 展开更多
关键词 GLIOBLASTOMA Forkhead box protein O1(FOXO1) MiR-506 e26 transformation specific-1(eTS1) CHeMOSeNSITIVITY
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