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PRMT5 mediated H4R3sme2 confers cell differentiation in Pediatric Acute B-Lymphoblastic Leukemia

ABSTRACT: To gain insight into the molecular mechanisms involved in the regulation of PRMT5 in human leukemic cells, microarray analysis was performed in NALM6 cell. Upon PRMT5 knockdown, 40 genes were highly expressed and 18 genes were downregulated (cut off fold induction > 0.8 or < -0.8, P<0.05). Potential target genes of PRMT5 were screened in B-ALL cells by microarray, and identified in B-ALL cells by quantitative real-time PCR (qRT-PCR) and chromatin immunoprecipitation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE108433 | GEO | 2017/12/23

SECONDARY ACCESSION(S): PRJNA427273

REPOSITORIES: GEO

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PRMT5 mediated H4R3sme2 confers cell differentiation in Pediatric Acute B-Lymphoblastic Leukemia

Project description:PRMT5 mediated H4R3sme2 confers cell differentiation in Pediatric Acute B-Lymphoblastic Leukemia

| PRJNA427273 | ENA

RNA deep sequencing to compare genome-wide differences between PRMT5/knockdown and control AML cells

Project description:We report the pro-leukemic activities of PRMT5 in AML partly via modulating the transcription of key genes. The goal of this experiment is to confirm the changes observed in expression of genes targeted by PRMT5 activities. RNA Deep sequencing was employed to validate and reproduce the changes measured by quantitative reverse transcription polymerase chain reaction (qRTâPCR) techniques. Total RNA samples from MV4-11 cell line (FLT3-ITD AML) following PRMT5 knockdown using specific short hairpin RNA (shRNA) was used to compare gene expression pattern between PRMT5/Knockdown and control (control: MV4-11 cells transduced with scramble control).

2016-05-19 | E-GEOD-75215 | biostudies-arrayexpress

RNA deep sequencing to compare genome-wide differences between PRMT5/knockdown and control AML cells

2016-05-19 | GSE75215 | GEO

PRMT5 is essential for sustaining normal adlut hematopoiesis

Project description:Examining the effects of PRMT5 loss on the gene expression profile of hematopoietic stem and progenitor cells We established the PRMT5 conditional KO mice, and bred the mice with Mx1 cre transgenic mice to delete PRMT5 in hematopoietic cells. We isolated hematopoetic stem and progenitor cells 3 days after PRMT5 deletion, and examined the gene expression files using RNA-sequencing.

2015-07-15 | E-GEOD-69937 | biostudies-arrayexpress

ChIP-on-chip from MDA-MB-231 cells with PHF1, CUL4B and PRMT5

Project description:It has been reported that PHF1, CUL4B and PRMT5 all play important roles in epigenetic regulation. We reported that PHF1, CRL4B and PRMT5 may act as a complex in transcriptional regulation and have a vital effect in breast cancer progression. So we performed ChIP-on-chip assays to find unique promoters co-targeted by PHF1, CUL4B and PRMT5. PHF1, CUL4B and PRMT5 have a predominant cooperation, at least in MDA-MB-231 cells. comparison of PHF1, CUL4B and PRMT5 target genes

2016-07-07 | E-GEOD-84071 | biostudies-arrayexpress

PRMT5 genomic deregulation supports growth and stress tolerance in chronic lymphocytic leukemia

Project description:Patients suffering from chronic lymphocytic leukemia (CLL) display highly diverse clinical courses ranging from indolent cases to aggressive disease with genetic and epigenetic features resembling this diversity. Here, we developed a comprehensive approach combining a variety of molecular and clinical data to identify translocation events disrupting long-range chromatin interactions and causing cancer-relevant transcriptional deregulation. Thereby, we identified a B cell specific cis-regulatory element restricting the expression of genes in the associated locus, including PRMT5 and DAD1, two factors with oncogenic potential. Examining the role of PRMT5 in CLL identified transcriptional programs associated with pathways of stress tolerance and growth support, maintaining MYC-driven gene expression in vivo and in vitro. Conversely, inhibition of PRMT5 impairs factors involved in DNA-repair and sensitizes cells for apoptosis. Finally, we show that artificial deletion of the regulatory element from its endogenous context resulted in upregulation of corresponding genes, including PRMT5. Furthermore, such disruption renders PRMT5 transcription vulnerable to additional stimuli and subsequently also alters the expression of downstream PRMT5 targets.

2020-08-19 | E-MTAB-8219 | biostudies-arrayexpress

PRMT5 genomic deregulation supports growth and stress tolerance in chronic lymphocytic leukemia

2020-08-19 | E-MTAB-8203 | biostudies-arrayexpress

Testing gene expression changes in VCaP cells following PRMT5 knockdown

Project description:VCaP cells expressing either NTC shRNA or PRMT5 shRNA 1 or shRNA 2 were treated with 100ng/ml doxycycline for 5 days This experiment is designed to see which genes and pathways are modulated by PRMT5 knockdown in VCaP cells VCaP cells were treated with 100ng/ml doxyxycline for 3 days.

2015-04-15 | E-GEOD-65965 | biostudies-arrayexpress

PRMT5 Modulates Splicing in Hematopoietic Stem Cells

Project description:This study aimed to clarify the role of PRMT5 in the hematopoietic stem cell (HSC) compartment, and elucidate the functional relevance of PRMT5-mediated splicing in HSCs. We confirm the cell intrinsic requirement for PRMT5 in HSC maintenance, and present evidence suggesting that PRMT5 deficiency perturbs HSC proteostasis. Notably, we also uncover a critical role for PRMT5 in maintaining HSC genomic integrity by modulating splicing of genes involved in DNA repair; loss of which leads to unresolved DNA damage, p53 activation and rapid HSC exhaustion. Overall, these findings establish PRMT5-mediated splicing as a major determinant of HSC fate, and highlight the need to maintain an adequate level of PRMT5 activity in HSCs.

2019-03-03 | GSE116674 | GEO

PRMT5 knockdown changes gene expression in prostate cancer cells

Project description:PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine. Recent reports have indicated that PRMT5 is overexpressed in multiple cancer types, including prostate. However, the exact contribution of PRMT5 to prostate tumorigenesis is unknown. To explore the functional role of PRMT5 in prostate cancer (PCa), we knocked down PRMT5 by lentiviral shRNAs in both AR-dependent LNCaP cells and AR-independent PC3 cells. Our data suggests that PRMT5 regulates PCa cell biology. To further identify PRMT5-regulated genes in PCa, we performed paired-end RNA-seq analysis in PC3 and LNCaP cells with or without PRMT5-knockdown.

2023-12-25 | GSE117596 | GEO

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