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您的检索式：作者名="Chencheng Han"
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| 1 | LncRNA LINC00525 suppresses p21 expression viamRNA decay and triplex-mediated changes in chromatin structure in lung adenocarcinoma显示文摘Background:Emerging evidence suggests that long noncoding RNAs(lncRNAs)play crucial roles in various cancers.In the present study,we aim to investigate the function and molecular mechanism of an up-regulated and survivalassociated lncRNA,LINC00525,in lung adenocarcinoma(LUAD).Methods:The expression level of LINC00525 in tissueswas determined by quantitative reverse transcription polymerase chain reaction(RT-qPCR)and in situ hybridization(ISH).The functional role of LINC00525 in LUAD was investigated using gain-and loss-of-function approaches,both in vivo and in vitro.RNA pull-down,RNA immunoprecipitation(RIP),chromatin immunoprecipitation(ChIP),triplex-capture assay,dual-luciferase assay,gene expression microarray,and bioinformatics analysis were used to investigate the potential underlying mechanisms involved.Results:LINC00525 is highly expressed in LUAD cells and tissues.Survival analysis indicated that upregulation of LINC00525 was associated with poor prognosis in patients with LUAD patients.Knockdown of LINC00525 inhibited cell proliferation and cell cycle progression in vitro.In xenograft models,LINC00525 knockdown suppressed tumor growth and tumorigenesis of tumorbearing mice.Mechanistically,LINC00525 epigenetically suppressed p21 transcription by guiding Enhancer Of Zeste 2 Polycomb Repressive Complex 2 Subunit(EZH2)to the p21 promoter through an formation of RNA-DNA triplex with the p21 promoter,leading to increased trimethylation of lysine 27 on histone 3(H3K27me3)of the p21 promoter.In addition,LINC00525 repressed p21 expression post-transcriptionally by enhancing p21mRNA decay.LINC00525 promoted p21mRNAdecay by competitively binding toRNABindingMotif Single Stranded Interacting Protein 2(RBMS2).Conclusion:Our findings demonstrate that LINC00525 promotes the progression of LUAD by reducing the transcription and stability of p21 mRNA in concert with EZH2 and RBMS2,thus suggesting that LINC00525 may be a potential therapeutic target for clinical intervention in LUAD. | Panqi Fang Hao Chen Zhifei Ma Chencheng Han Wenda Yin Siwei Wang Hongyu Zhu Wenjia Xia Jie Wang Lin Xu Tongyan Liu Rong Yin | 2021 | Cancer Communications2021，41，7： | 2 |
| 2 | Dyssynchrony Induced by Ventricular Preexcitation: A Risk Factor for the Development of Dilated Cardiomyopathy显示文摘Background:Signifi cant left ventricular dysfunction may arise in right-sided accessory pathways with ventricular preexcitation in the absence of recurrent or incessant tachycardia.This has just been realized and not enough attention has been paid to it.Methods:In the last 7 years,we identifi ed 12 consecutive children with a diagnosis of ventricular preexcitation–induced dilated cardiomyopathy.This report describes the clinical and echocardiographic characteristics of the patients before and after ablation.Results:Dyssynchronous ventricular contraction was observed by M-mode echocardiography and two-dimensional strain analysis in all patients.The basal and middle segments of the interventricular septum became thin and moved similarly to an aneurysm,with typical bulging during the end of systole.The locations of the accessory pathways were the right-sided septum(n=5)and the free wall(n=7).Left ventricular synchrony was obtained shortly after ablation.The left ventricular function recovered to normal and the left ventricular end-diastolic diameter decreased gradually during follow-up.Conclusions:A causal relationship between ventricular preexcitation and the development of dilated cardiomyopathy is supported by the complete recovery of left ventricular function and reversed left ventricular remodeling after the loss of ventricular preexcitation.Preexcitation-related dyssynchrony was thought to be the crucial mechanism.Ventricular preexcitation–induced dilated cardiomyopathy is an indication for ablation with a good prognosis. | Chencheng Dai Baojing Guo Ling Han Caihua Sang Jianzeng Dong Changsheng Ma | 2020 | Cardiovascular Innovations and Applications2020，，3： | 0 |
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