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The long non-coding RNA HOTAIRM1 promotes tumor aggressiveness and radiotherapy resistance in glioblastoma

ABSTRACT: The long non-coding RNA HOTAIRM1 promotes tumor aggressiveness and radiotherapy resistance in glioblastoma

PROVIDER: PRJNA638410 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11968776_1.fastq.gz	Fastqsanger.gz
	SRR11968776_2.fastq.gz	Fastqsanger.gz
	SRR11968777_1.fastq.gz	Fastqsanger.gz
	SRR11968777_2.fastq.gz	Fastqsanger.gz
	SRR11968778_1.fastq.gz	Fastqsanger.gz

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The long non-coding RNA HOTAIRM1 promotes tumor aggressiveness and radiotherapy resistance in glioblastoma

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

The long non-coding RNA HOTAIRM1 promotes tumor aggressiveness and radiotherapy resistance in glioblastoma

2020-06-10 | GSE152147 | GEO

Combined anti-C1-INH and Radiotherapy against Glioblastoma

Project description:Animals with intracranial glioblastoma of the NS1 cells line were treated with anti-C1-INH +/- radiotherapy or were untreated control animals.

2022-10-19 | E-MTAB-12296 | biostudies-arrayexpress

The long non-coding RNA HOTAIRM1 promotes tumor aggressiveness and radiotherapy resistance in glioblastoma.

Project description:Glioblastoma is the most common malignant primary brain tumor. To date, clinically relevant biomarkers are restricted to isocitrate dehydrogenase (IDH) gene 1 or 2 mutations and O6-methylguanine DNA methyltransferase (MGMT) promoter methylation. Long non-coding RNAs (lncRNAs) have been shown to contribute to glioblastoma pathogenesis and could potentially serve as novel biomarkers. The clinical significance of HOXA Transcript Antisense RNA, Myeloid-Specific 1 (HOTAIRM1) was determined by analyzing HOTAIRM1 in multiple glioblastoma gene expression data sets for associations with prognosis, as well as, IDH mutation and MGMT promoter methylation status. Finally, 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, decreased invasive growth and diminished colony formation capacity upon HOTAIRM1 down-regulation. Integrated proteogenomic analyses revealed impaired mitochondrial function and determination of reactive oxygen species (ROS) levels confirmed increased ROS levels upon HOTAIRM1 knock-down. HOTAIRM1 knock-down decreased expression of transglutaminase 2 (TGM2), 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 both 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.

| S-EPMC8478910 | biostudies-literature

Transcription profiling of human glioblastoma samples from a homogenous cohort of patients treated within clinical trial with eitehr radiotherapy or radiotherapy and temonzolomide

Project description:Analysis of 80 glioblastoma specimen of patients treated within clinical trials and 4 samples of "normal" brain tissue (non-tumoral). The data was used to identify factors of resistance to a chemoradiation therapy protocol of radiotherapy and concomitant and adjuvant temozolomide (alkylating agent). Experiment Overall Design: 80 glioblastoma specimen and 4 non-tumoral brain samples

2008-10-18 | E-GEOD-7696 | biostudies-arrayexpress

Long Intergenic Non-Coding RNA HOTAIRM1 Regulates Cell Cycle Progression During Myeloid Maturation in NB4 Promyelocytic Leukemia Cells

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

lncRNA HOTAIRM1 Facilitates Nasopharyngeal Carcinoma Resistance to Irradiation and Ferroptosis by Increasing SLC7A11 Stability and Expression via METTL3-mediated m6A Methylation

Project description:Radiotherapy has become a main treatment for patients with nasopharyngeal carcinoma (NPC), who often develop residual or recurrent tumors due to radioresistance. The lncRNA HOTAIRM1 plays crucial roles in the formation and development of various cancers, but the interaction between HOTAIRM1 and radioresistant NPC remains unclear. In this study, we evaluated the potential of HOTAIRM1 as a biomarker of NPC radioresistance. Proliferation, apoptosis, DNA damage, and RNA-seq analyses were conducted to examine the mechanisms by which HOTAIRM1 contributes to NPC radioresistance, and in vivo experiments were performed using nude mice. Our findings indicated that HOTAIRM1 levels were upregulated in radioresistant NPC tissues and cell lines. High HOTAIRM1 expression was associated with increased NPC cell proliferation, decreased apoptosis, and decreased cellular DNA damage after radiotherapy. Mechanistically, HOTAIRM1 promoted NPC radioresistance by increasing SLC7A11 stability and expression through METTL3-mediated m6A demethylation. Additionally, high HOTAIRM1 expression decreased SLC7A11-associated ferroptosis. Our findings demonstrate that HOTAIRM1 promotes METTL3-mediated m6A methylation to increase SLC7A11 expression and stability, thereby inhibiting ferroptosis to trigger NPC radioresistance. This novel molecular mechanism underlying the role of HOTAIRM1 in the regulation of radioresistant NPC may aid in the identification of biomarkers and therapeutic targets for the treatment of radioresistant NPC.

2023-04-12 | GSE229333 | GEO

Long Intergenic Non-Coding RNA HOTAIRM1 Regulates Cell Cycle Progression During Myeloid Maturation in NB4 Promyelocytic Leukemia Cells

2014-04-30 | GSE49516 | GEO

Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy [ChIP-Seq]

Project description:This study examines the reorganization of transcriptionally active chromatin that underlies the adaptive response of glioblastoma cells to radiotherapy.

2023-12-01 | GSE211147 | GEO

Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy [ATAC-Seq]

Project description:This study examines the reorganization of transcriptionally active chromatin that underlies the adaptive response of glioblastoma cells to radiotherapy.

2023-12-01 | GSE211148 | GEO

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