Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA317566 | ENA |
REPOSITORIES: ENA
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Project description:LIN28B is overexpressed in specific subtypes of pediatric leukemia and regulates lncRNA H19
| PRJNA317558 | ENA
Project description:LIN28B is overexpressed in specific subtypes of pediatric leukemia and regulates lncRNA H19 [Oci-AML3]
| PRJNA317567 | ENA
Project description:The stem cell gene LIN28B was recently shown to be overexpressed in a foetal-like subgroup of juvenile myelomonocytic leukaemia. Given the involvement of LIN28B in a variety of solid paediatric cancers, we conducted a meta-analysis of LIN28B levels using publicly available gene expression data of 1361 paediatric leukaemia samples. Interestingly, this analysis revealed LIN28B overexpression in 102 childhood leukaemia patients (7.5%), suggesting oncogenic activity for LIN28B in the context of paediatric haematological diseases. As the mode of action of LIN28B during normal and malignant haematopoiesis remains largely unexplored, we subsequently analysed the transcriptional consequences of LIN28B modulation on normal and malignant haematopoietic cells and identified the long non-coding RNA (lncRNA) H19 as the first LIN28B-regulated lncRNA. K562 cells were retrovirally transduced with shRNA GN36578 against LIN28B and a shRNA-miR non-targeting control TRH1103 (both Transomic), selected with puromycin and hybridized on Agilent microarray.
2016-04-07 | E-GEOD-79980 | biostudies-arrayexpress
Project description:The stem cell gene LIN28B was recently shown to be overexpressed in a foetal-like subgroup of juvenile myelomonocytic leukaemia. Given the involvement of LIN28B in a variety of solid paediatric cancers, we conducted a meta-analysis of LIN28B levels using publicly available gene expression data of 1361 paediatric leukaemia samples. Interestingly, this analysis revealed LIN28B overexpression in 102 childhood leukaemia patients (7.5%), suggesting oncogenic activity for LIN28B in the context of paediatric haematological diseases. As the mode of action of LIN28B during normal and malignant haematopoiesis remains largely unexplored, we subsequently analysed the transcriptional consequences of LIN28B modulation on normal and malignant haematopoietic cells and identified the long non-coding RNA (lncRNA) H19 as the first LIN28B-regulated lncRNA. Oci-AML3 cells were retrovirally transduced with MSCV-PIG-LIN28B and MSCV-PIG-empty vectors (gifts from Johua Mendel lab), selected with puromycin and hybridized on Agilent microarray.
2016-04-07 | E-GEOD-79979 | biostudies-arrayexpress
Project description:The stem cell gene LIN28B was recently shown to be overexpressed in a foetal-like subgroup of juvenile myelomonocytic leukaemia. Given the involvement of LIN28B in a variety of solid paediatric cancers, we conducted a meta-analysis of LIN28B levels using publicly available gene expression data of 1361 paediatric leukaemia samples. Interestingly, this analysis revealed LIN28B overexpression in 102 childhood leukaemia patients (7.5%), suggesting oncogenic activity for LIN28B in the context of paediatric haematological diseases. As the mode of action of LIN28B during normal and malignant haematopoiesis remains largely unexplored, we subsequently analysed the transcriptional consequences of LIN28B modulation on normal and malignant haematopoietic cells and identified the long non-coding RNA (lncRNA) H19 as the first LIN28B-regulated lncRNA.
2016-04-07 | GSE79980 | GEO
Project description:The stem cell gene LIN28B was recently shown to be overexpressed in a foetal-like subgroup of juvenile myelomonocytic leukaemia. Given the involvement of LIN28B in a variety of solid paediatric cancers, we conducted a meta-analysis of LIN28B levels using publicly available gene expression data of 1361 paediatric leukaemia samples. Interestingly, this analysis revealed LIN28B overexpression in 102 childhood leukaemia patients (7.5%), suggesting oncogenic activity for LIN28B in the context of paediatric haematological diseases. As the mode of action of LIN28B during normal and malignant haematopoiesis remains largely unexplored, we subsequently analysed the transcriptional consequences of LIN28B modulation on normal and malignant haematopoietic cells and identified the long non-coding RNA (lncRNA) H19 as the first LIN28B-regulated lncRNA.
2016-04-07 | GSE79979 | GEO
Project description:To investigate the role of lncRNA H19 in glioma, transcriptome analysis was performed on H19 overexpressed, knocked down, and control groups in U87MG and A172.
2024-07-31 | GSE243116 | GEO
Project description:Dystrophin proteomic regulation in Muscular Dystrophies (MD) remains unclear. We report that a long noncoding RNA (lncRNA) H19 associates with dystrophin. To investigate the biological roles of this interaction in vivo, we performed mass spectrometry analysis of dystrophin and its associated proteins in H19-proficient and -deficient C2C12 myotubes. Mass spectrometry data indicated that in H19-proficient myotubes, dystrophin associates with components of dystrophin-associated protein complex (DPC); however, in H19-deficient myotubes, dystrophin associated with UBA1, UB2G1, TRIM63 ubiquitin E3 ligase and ubiquitin. In H19-deficient myotubes, dystrophin was post-translationally modified with K48-linked poly-ubiquitination at Lys3577 (referred to as Ub-DMD). This mass spectrometry study demonstrated that lncRNA H19, associates with dystrophin and inhibits E3 ligase-dependent Ub-DMD formation and its subsequent proteasomal degradation. Based on this study, H19 RNA oligonucleotides conjugated with a muscle homing ligand Agrin (referred to as AGR-H19) and Nifenazone, a TRIM63-specific small molecule inhibitor, reverses the dystrophin degradation in iPSC-derived skeletal muscle cells from Becker Muscular Dystrophy patients. Furthermore,treatment of mdx mice with exon-skipping reagent, in combination with either AGR-H19 or Nifenazone, dramatically stablized dystrophin, preserved skeletal/cardiac muscle histology, and improved strength/heart function. In summary, this mass spectrometry study paves the way to meaningful targeted therapeutics for BMD and certain DMD patients.
2020-08-19 | PXD020566 | Pride
Project description:Long non-coding RNAs (lncRNAs) constitute a significant portion of the human genome. LncRNA H19 is among the first identified lncRNAs and is highly expressed during fetal development but decreases in the liver shortly after birth. H19 is reactivated during the development of various liver diseases; however, the role of H19 in the pathogenesis of alcohol-associated liver disease (ALD) remains elusive. Elevated levels of H19 were observed in human peripheral blood and livers of patients with alcohol-associated cirrhosis and alcohol-associated hepatitis. Similar observations were also seen in the livers of ethanol-fed mice. Hepatic overexpression of H19 promoted ethanol-induced liver steatosis and injury. Metabolomics analysis revealed a significant decrease in methionine levels in H19-overexpressed mouse livers. H19 was found to inhibit Betaine-homocysteine methyltransferase (BHMT), a key enzyme in methionine synthesis. H19 regulated the alternative splicing process of Bhmt through Polypyrimidine tract-binding protein 1 (PTBP1), resulting in a decrease in the Bhmt protein-coding variant. Maternally specific knockout of H19 (H19Mat+/-) or liver-specific knockout of the H19 differentially methylation domain (H19DMDHep-/-) in ethanol-fed mice led to an increase in BHMT expression and improvement in hepatic steatosis. Additionally, restoration of BHMT rescued H19 overexpression-mediated ethanol-induced fatty liver. In summary, we identified a novel mechanism of H19 regulating BHMT alternative splicing and methionine metabolism through PTBP1 in ALD. Targeting the H19-PTBP1-BHMT pathway could be a potential therapeutic intervention in patients with ALD.
2025-05-01 | GSE267404 | GEO
Project description:Resistance to azacitidine represents a major obstacle in the treatment of acute myeloid leukemia (AML), yet the molecular mechanisms remain poorly understood. Long non-coding RNAs (lncRNAs) have been implicated in drug resistance across cancers, with H19 emerging as a promising candidate due to its oncogenic roles and association with adverse outcomes in AML. Here, we investigated whether H19 contributes to azacitidine resistance. Using K562 cells subjected to prolonged drug exposure, we established an azacitidine-resistant model that maintained proliferation and viability and resisted apoptosis under treatment. RNA sequencing revealed robust upregulation of H19 and its derived miR-675-3p/-5p in resistant cells, with similar induction of H19 in sensitive cells after extended azacitidine exposure. However, functional assays demonstrated that neither H19 overexpression in sensitive K562 and KG1a cells nor its downregulation in resistant cells altered proliferation, apoptosis, or drug response. These results suggest that H19 upregulation reflects epigenetic reprogramming during prolonged drug exposure but does not functionally drive resistance. Our findings refine the role of H19 in AML, highlighting the need to distinguish biomarkers of drug exposure from true mediators of resistance when identifying therapeutic targets in azacitidine-resistant AML.
2026-01-31 | GSE312727 | GEO