RNA-seq comparative analysis of HOTAIRM1 knockdown in Caki-1 cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA562846 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10038188.fastq.gz | Fastqsanger.gz | |||
| SRR10038189.fastq.gz | Fastqsanger.gz | |||
| SRR10038190.fastq.gz | Fastqsanger.gz | |||
| SRR10038191.fastq.gz | Fastqsanger.gz | |||
| SRR10038192.fastq.gz | Fastqsanger.gz |
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Project description:RNA-seq comparative analysis of HOTAIRM1 knockdown in Caki-1 cells
2019-12-31 | GSE136604 | GEO
Project description:To investigate the target genes of HOTAIRM1 in glioma cells, we conducted a lncRNA + mRNA expression microarray analysis to identify novel HOTAIRM1 regulating genes. Three glioma cell lines U87MG, T98G and A172 stably knockdown HOTAIRM1 were used as the experiments models. We conservatively established a minimum of 2-fold difference between shHOTAIRM1 (knockdown HOTAIRM1) and shNT (control group), and identified 10 up-regulated and 22 down-regulated genes that met the threshold in all cell lines.
2021-12-26 | GSE192627 | GEO
Project description:HOTAIRM1 is a long intergenic non-coding RNA located in the human HOXA gene cluster, with gene expression highly specific for maturing myeloid cells, particularly during all-trans retinoic acid (ATRA) induction of granolopoiesis in NB4, a human t(15;17) acute promyelocytic leukemia (APL) cell line. We sought to assess the impact of HOTAIR knockdown on the global programme of gene expression underlying the granulocytic maturing process in NB4 cells. The knockdown of HOTAIRM1 resulted in a less differentiated expression profile in the NB4 cells after 4 days of ATRA-induced granulocytic differentiation, with retained expression of many otherwise ATRA-suppressed cell cycle and DNA replication genes, as well as abated induction of cell surface leukocyte activation and defense response genes. The shRNA expressing vector targeting the HOTAIRM1 transcript and the control vector expressing scrambled shRNA sequence were generated based on the pLKO.3G vector backbone (Addgene). The stable cell lines derived from NB4 cells transfected with lentiviral vectors were selected by FACS sorting of GFP selection marker positive cells and isolation of single cell derived clones on soft agar plates. Biologically duplicated total RNA samples were prepared from HOTAIRM1 knockdown and the scrambled shRNA expressing control cells, plus one total RNA from each of wild type NB4 cells and HOTAIRM1 knockdown (by a different shRNA construct) cells, before and after 96 hours of ATRA (0.5 uM) induced granulocytic differentiation.
2014-04-30 | E-GEOD-49516 | biostudies-arrayexpress
Project description:The eukaryotic RNA processing factor Y14 participates in double-strand break (DSB) repair via its RNA-dependent interaction with the non-homologous end-joining (NHEJ) complex. We identified the long non-coding RNA HOTAIRM1 as a candidate that mediates this interaction. HOTAIRM1 localized to DNA damage sites induced by ionizing radiation. Depletion of HOTAIRM1 delayed the recruitment of DNA damage response and repair factors to DNA lesions and reduced DNA repair efficiency. Identification of the HOTAIRM1 interactome revealed a large set of RNA processing factors including mRNA surveillance factors. The surveillance factors Upf1 and SMG6 localized to DNA damage sites in a HOTAIRM1-dependent manner. Depletion of Upf1 or SMG6 increased the level of DSB-induced non-coding transcripts at damaged sites, indicating a pivotal role for Upf1/SMG6-mediated RNA degradation in DNA repair. We conclude that HOTAIRM1 serves as an assembly scaffold for both DNA repair and RNA processing factors that act in concert to repair DSBs.
2023-05-10 | PXD034470 | Pride
Project description:Glioblastoma is the most common malignant primary brain tumor. Clinically relevant biomarkers are restricted to isocitrate dehydrogenase (IDH) gene 1 or 2 mutation and O6-methylguanine DNA methyltransferase (MGMT) promoter methylation. Long non-coding RNA (lncRNA) alterations may contribute to glioblastoma pathogenesis and potentially serve as novel biomarkers. The clinical significance of HOXA Transcript Antisense RNA, Myeloid-Specific 1 (HOTAIRM1) was analyzed in multiple glioblastoma gene expression data sets for associations with prognosis and IDH mutation and MGMT promoter methylation status. The role of HOTAIRM1 in glioblastoma biology and radiotherapy resistance was characterized in vitro and in vivo. We identified HOTAIRM1 as a candidate lncRNA whose up-regulation is significantly associated with shorter survival of glioblastoma patients independent from IDH mutation and MGMT promoter methylation. Glioblastoma cell line models uniformly showed reduced cell viability, less invasive growth and diminished colony formation capacity upon HOTAIRM1 down-regulation. Integrated proteogenomic analyses and determination of reactive oxygen species (ROS) levels revealed impaired mitochondrial function and increased ROS levels upon HOTAIRM1 knock-down. HOTAIRM1 knock-down decreased expression of transglutaminase 2 (TGM2) as a candidate protein implicated in mitochondrial function, and knock-down of TGM2 mimicked the phenotype of HOTAIRM1 down-regulation in glioblastoma cells. Moreover, HOTAIRM1 modulates radiosensitivity of glioblastoma cells in vitro and in vivo. Our data support a role for HOTAIRM1 as a driver of biological aggressiveness, radioresistance and poor outcome in glioblastoma. Targeting HOTAIRM1 may be a promising new therapeutic approach.
2022-01-19 | PXD020141 | Pride
Project description:Glioblastoma is the most common malignant primary brain tumor. Clinically relevant biomarkers are restricted to isocitrate dehydrogenase (IDH) gene 1 or 2 mutation and O6-methylguanine DNA methyltransferase (MGMT) promoter methylation. Long non-coding RNA (lncRNA) alterations may contribute to glioblastoma pathogenesis and potentially serve as novel biomarkers. The clinical significance of HOXA Transcript Antisense RNA, Myeloid-Specific 1 (HOTAIRM1) was analyzed in multiple glioblastoma gene expression data sets for associations with prognosis and IDH mutation and MGMT promoter methylation status. The role of HOTAIRM1 in glioblastoma biology and radiotherapy resistance was characterized in vitro and in vivo. We identified HOTAIRM1 as a candidate lncRNA whose up-regulation is significantly associated with shorter survival of glioblastoma patients independent from IDH mutation and MGMT promoter methylation. Glioblastoma cell line models uniformly showed reduced cell viability, less invasive growth and diminished colony formation capacity upon HOTAIRM1 down-regulation. Integrated proteogenomic analyses and determination of reactive oxygen species (ROS) levels revealed impaired mitochondrial function and increased ROS levels upon HOTAIRM1 knock-down. HOTAIRM1 knock-down decreased expression of transglutaminase 2 (TGM2) as a candidate protein implicated in mitochondrial function, and knock-down of TGM2 mimicked the phenotype of HOTAIRM1 down-regulation in glioblastoma cells. Moreover, HOTAIRM1 modulates radiosensitivity of glioblastoma cells in vitro and in vivo. Our data support a role for HOTAIRM1 as a driver of biological aggressiveness, radioresistance and poor outcome in glioblastoma. Targeting HOTAIRM1 may be a promising new therapeutic approach.
2020-06-10 | GSE152147 | GEO
Project description:HOTAIRM1 is a long intergenic non-coding RNA located in the human HOXA gene cluster, with gene expression highly specific for maturing myeloid cells, particularly during all-trans retinoic acid (ATRA) induction of granolopoiesis in NB4, a human t(15;17) acute promyelocytic leukemia (APL) cell line. We sought to assess the impact of HOTAIR knockdown on the global programme of gene expression underlying the granulocytic maturing process in NB4 cells. The knockdown of HOTAIRM1 resulted in a less differentiated expression profile in the NB4 cells after 4 days of ATRA-induced granulocytic differentiation, with retained expression of many otherwise ATRA-suppressed cell cycle and DNA replication genes, as well as abated induction of cell surface leukocyte activation and defense response genes.
2014-04-30 | GSE49516 | GEO
Project description:Although a majority of breast cancers (BrCa) are Estrogen receptor-alpha (ERa)-positive, existing endocrine therapies that target ERa can lead to hormone-resistant disease. The mechanisms of how normal breast epithelium is transformed into malignant remain poorly defined, and a deeper understanding is needed to design novel therapeutics. Several epigenetic regulators including long non-coding RNAs (lncRNAs) are aberrantly expressed in BrCa, resulting in abnormal gene expression patterns and tumor growth. Here, we show that HOTAIRM1, which we previously defined as a p53-regulated lncRNA in human stem cells, acts as a tumor suppressor to counteract ERa-activity in BrCa. Global expression analyses uncovered a significant correlation between reduced HOTAIRM1 expression and poor survival of ER+ BrCa patients. Promoter DNA methylation and histone mark enrichment revealed that HOTAIRM1 is epigenetically silenced in BrCa patients and cell lines. We found that HOTAIRM1 depletion promotes, whereas exogenous HOTAIRM1 reduces survival and proliferation of BrCa cells. Guilt by association analysis in BrCa patients, combined with HOTAIRM1-dependent transcriptome profiling in BrCa cells reveal that HOTAIRM1 expression negatively correlates with proteins involved in ERa-activity and estrogen response. An unbiased profiling of HOTAIRM1-interactome show that HOTAIRM1 interacts with pioneer factor FOXA1 in ER+ BrCa cells. Further, our global ER/FOXA1 chromatin enrichment profiling in response to estrogen demonstrate increased enrichment of ER and FOXA1 to estrogen response elements (EREs) that results in significantly higher expression of ERa-targets in absence of HOTAIRM1. Thus, HOTAIRM1 suppresses ERa-activity in BrCa by restricting chromatin accessibility of pioneer factor FOXA1. To our knowledge, our results are the first to define a non-proteomic component that disrupts the activity of a pioneer factor in order to achieve tumor suppression
2023-08-15 | GSE135894 | GEO
Project description:To compare the transcriptomic changes mediated by VHL knockout in Caki-1 cells, we carried out the next-generation sequencing (NGS)-derived transcriptomic profiling. We found significant enrichment of gene signatures involving IFNa/b signaling in VHL-KO Caki-1 cells compared to control cells. Our analysis also demonstrated that VHL deficiency induced the expression of genes associated with the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway involved in sensing the cytoplasmic presence of double-stranded DNA (dsDNA).
2024-08-10 | GSE196509 | GEO