Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1213289 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:LncRNA ENO1-IT1 has been found to be mainly located in the nucleus of colorectal mucosa epithelial cells, which indicates that this lncRNA may be responsible for regulating the expression of target gene. To address whether ENO1-IT1 modulates epigenetic changes genome-wide, we performed chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) in HCT116 cells
2022-10-25 | GSE139403 | GEO
Project description:ENO1 (α-Enolase 1) is a key glycolytic enzyme that catalyzes the dehydratation of 2-phosphoglycerate to phosphoenolpyruvate. It also belongs to a member of the RNA degradosome of Escherichia coli and facilitates RNA degradation, but it’s currently unknown whether ENO1 possesses similar function in eukaryotes. To test this possibility,we performed RNA-seq assays expressing NTC or ENO1 shRNA, respectively.
2021-09-10 | GSE153989 | GEO
Project description:Enolase 1 (ENO1) is a glycolytic enzyme that plays essential roles in various pathological activities including cancer development. However, the mechanisms underlying ENO1-contributed tumorigenesis are not well explained. Here, we uncover that ENO1, as an RNA-binding protein, binds to the cytosine-uracil-guanine-rich elements of YAP1 messenger RNA to promote its translation. ENO1 and YAP1 positively regulate alternative arachidonic acid (AA) metabolism by inverse regulation of PLCB1 and HPGD (15-hydroxyprostaglandin dehydrogenase). The YAP1/PLCB1/HPGD axis-mediated activation of AA metabolism and subsequent accumulation of prostaglandin E2 (PGE2) are responsible for ENO1-mediated cancer progression, which can be retarded by aspirin. Finally, aberrant activation of ENO1/YAP1/PLCB1 and decreased HPGD expression in clinical hepatocellular carcinoma samples indicate a potential correlation between ENO1-regulated AA metabolism and cancer development. These findings underline a new function of ENO1 in regulating AA metabolism and tumorigenesis, suggesting a therapeutic potential for aspirin in patients with liver cancer with aberrant expression of ENO1 or YAP1.
2023-05-19 | GSE183703 | GEO
Project description:We systematically evaluated the expression pattern and function of ENO1 in AML. Knockdown ENO1 significantly inhibited ERK pathway phosphorylation, ERK pathway inhibitors significantly inhibited proliferation, clonal formation, migration and invasion of AML cells in vitro, blocked cell cycle and promoted apoptosis of AML cells, and activators of ERK pathway could reverse the effects of knockdown ENO1 on AML cells. The results showed that knockdown ENO1 inhibited the proliferation and invasion of AML cells in mice by inhibiting the activation of ERK pathway, and induced a significant increase in the overall survival rate of mice. Overall, this study aims to explore the role of ENO1 in the development and progression of AML and its potential mechanism, in order to provide a potential target for the treatment of AML.
2024-07-30 | GSE272844 | GEO
Project description:HeLa cells were either treated with ENO1 or control siRNAs using the protocol of the RNAiMax reagent (ENO1 pool: SMARTpool ON-TARGETplus L-004034-00-0005 and control pool: ON-TARGETplus non-targeting siRNAs 1-4). Three replicates per condition were produced.
2020-10-27 | E-MTAB-9032 | biostudies-arrayexpress
Project description:We systematically evaluated the expression pattern and function of ENO1 in BL and clarified that ENO1, regulated by cMyc, can promote BL cell proliferation and metastasis by activating TGFβ1 signaling pathways in a plasmin-mediated manner. Through structure-based virtual screening, we successfully discovered Ciwujianoside E (L-06) as a novel ENO1 inhibitor which can limit BL cell proliferation and dissemination in vitro and in vivo.
2024-06-18 | GSE225685 | GEO
Project description:To demonstrate RIPSeeker program that is developed for RIP-seq analyses, we generated RIP-seq data corresponding to the protein CCNT1 in HEK293 cell line using standard RIP-seq protocols described in Zhao et al., (2010). We performed two in-house RIP-seq experiments both for CCNT1 in human HEK293 cells. Briefly, we generated tagged CCNT1 using a triple tag system that supports lentiviral stable expression and mammalian affinity purification (MAPLE) Mak et al (2010). The HEK293 cells stably expressing tagged CCNT1 was purified by M2 agarose beads, followed by RNA extraction by Trizol. The library synthesis was carried out according to the RIP-seq protocol described in Zhao et al., (2010) except that one of the two experiments was done with non-strand-specific sequencing.
2012-12-28 | E-GEOD-43170 | biostudies-arrayexpress
Project description:Background: Our former study demonstrated that anti-trophoblast antibodies (ATAB) are more prevalent in the sera of patients with unexplained recurrent miscarriages (uRM), and the detection of ATAB is restricted to binding to JEG-3 cells and the quantification by flow cytometry. We further proved that the ATAB-positive sera decrease the production of β-hCG and progesterone in the same cell model. The specific antigenic epitopes of ATAB are still unclear, therefore our aim was to identify one specific target of ATAB in uRM patients. Methods: The possible targets of ATAB were identified by western blots and mass spectrometry, and α-Enolase (ENO1) was further confirmed by a competition assay. The level of anti-ENO1 antibodies in the sera and the production of β-hCG and progesterone were evaluated with enzyme-linked immunosorbent assay (ELISA). Additionally, the expression of ENO1 in the first trimester placenta was analyzed with immunohistochemistry and triple fluorescence staining in uRM patients and healthy controls. Findings: ENO1 was identified to be a prominent target of ATAB and anti-ENO1 antibodies can decrease the secretion of β-hCG and progesterone. The titer of anti-ENO1 antibodies was increased in the sera of ATAB-positive patients compared to ATAB-negative patients. Overexpression of ENO1 and co-expression of ENO1 and β-arrestin was found in the extra villous trophoblasts of uRM patients in the first trimester placenta. Interpretation: Anti-ENO1 antibody in the sera may be a novel autoimmune biomarker of uRM. Decreasing anti-ENO1 antibodies or inhibiting ENO1 expression might be a potential therapeutic treatment for uRM patients.
2019-03-05 | PXD012478 | Pride
Project description:To demonstrate RIPSeeker program that is developed for RIP-seq analyses, we generated RIP-seq data corresponding to the protein CCNT1 in HEK293 cell line using standard RIP-seq protocols described in Zhao et al., (2010).
2012-12-28 | GSE43170 | GEO