Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of overexpression of PHF19 in multiple myeloma cells [RNA-seq]

ABSTRACT: Effect of overexpression of PHF19 in multiple myeloma cells [RNA-seq]

PROVIDER: PRJNA930064 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23293980_1.fastq.gz	Fastqsanger.gz
	SRR23293980_2.fastq.gz	Fastqsanger.gz
	SRR23293981_1.fastq.gz	Fastqsanger.gz
	SRR23293981_2.fastq.gz	Fastqsanger.gz
	SRR23293982_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Effect of overexpression of PHF19 in multiple myeloma cells [RNA-seq]

Project description:To investigate the transcriptomic effect of PHF19 overexpression in MM cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of AMO1 cells with differential PHF19 expression.

2023-01-31 | GSE224200 | GEO

The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma (ChIP-seq)

Project description:We here report a PRC2-associated cofactor, PHD finger protein 19 (PHF19, also known as Polycomb-like 3), as a crucial mediator of tumorigenicity in multiple myeloma (MM). Using various MM models, we demonstrated a critical requirement of PHF19 for tumor growth in vitro and in vivo. Mechanistically, PHF19-mediated oncogenic effect relies on its PRC2-interacting and chromatin-binding functions. ChIP-Seq profiling showed a critical role for PHF19 in maintaining the H3K27me3 landscape. PHF19 depletion led to loss of broad H3K27me3 domains possibly due to impaired H3K27me3 spreading from CpG islands

2019-08-31 | GSE135890 | GEO

PHF19 Promotes Cell Growth and Confers Drug Resistance through EZH2 Phosphorylation in Multiple Myeloma

Project description:To determine the effect of overexpression PHF19 in ARP1 myeloma cells Drug resistance is a major reason for the recurrence of multiple myeloma (MM). In addition to genetic mutations, epigenetic abnormalities are involved in the whole process of MM relapse and drug resistance. In this study, we investigate the roles of polycomb like protein 19 (PHF19), a critical gene involved in the epigenetic regulation of gene expression, in the development of MM. The gene expression profiling (GEP) data shows that PHF19 is significantly up-regulated in MM cells and associated with shortened progression-free survival and overall survival in MM patients. PHF19 promotes MM cell growth both in vitro and in a subcutaneous xenograft mouse model. Up-regulated PHF19 is also associated with the development of resistance to multiple drugs, including bortezomib, in MM cells. Moreover, miR-15a can directly target PHF19 by binding to its 3'-UTR. Since miR-15a is down-regulated in MM cells, PHF19 is considered to be up-regulated due to loss of the suppression by miR-15a. The mechanistic investigations indicate that PHF19 can activate AKT which in turn leads to an increase in the phosphorylation of EZH2, a core component of PRC2 that mediates the histone H3K27 methylation. Subsequently suppresses histone H3K27 methylation and causes up-regulated expression of several anti-apoptotic genes, including BCL-xL, MCL-1 and HIF-1alpha. Moreover, PDK1 activation is significantly increased in PHF19 overexpressing MM cells.

2020-03-31 | GSE128406 | GEO

The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma (RNA-Seq)

Project description:Dysregulation of Polycomb Repressive Complex 2 (PRC2) promotes oncogenesis partly through its enzymatic function for inducing tri-methylation of histone H3 lysine 27 (H3K27me3). However, it remains to be determined how PRC2 activity is regulated in normal and diseased settings. We here report a PRC2-associated cofactor, PHD finger protein 19 (PHF19, also known as Polycomb-like 3), as a crucial mediator of tumorigenicity in multiple myeloma (MM). Overexpression and/or genomic amplification of PHF19 is found associated with malignant progression of MM and plasma cell leukemia, correlating to worse treatment outcomes. Using various MM models, we demonstrated a critical requirement of PHF19 for tumor growth in vitro and in vivo. Mechanistically, PHF19-mediated oncogenic effect relies on its PRC2-interacting and chromatin-binding functions. ChIP-Seq profiling showed a critical role for PHF19 in maintaining the H3K27me3 landscape. PHF19 depletion led to loss of broad H3K27me3 domains possibly due to impaired H3K27me3 spreading from CpG islands, which is reminiscent to the reported effect of an ‘onco’-histone mutation, H3K27-to-methionine (H3K27M). RNA-Seq-based transcriptome profiling in MM lines also demonstrated a requirement of PHF19 for optimal silencing of PRC2 targets, which include cell cycle inhibitors and interferon-JAK-STAT signaling genes critically involved in tumor suppression.

2019-08-31 | GSE136410 | GEO

The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma

Project description:The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma

| PRJNA560497 | ENA

Effect of PBX1 overexpression in PCM6 and MM1S myeloma cell lines

Project description:Multiple Myeloma is an incurable plasma cell malignancy with a poor survival rate that is usually treated with immunomodulatory drugs (iMiDs) and proteosome inhibitors (PIs). The malignant plasma cells quickly become resistant to these agents causing relapse and uncontrolled growth of resistant clones. From whole genome sequencing (WGS) and RNA sequencing (RNA-seq) studies, different high-risk translocation, copy number, mutational, and transcriptional markers have been identified. One of these markers, PHF19, epigenetically regulates cell cycle and other processes and has already been studied using RNA-seq. In this study a massive (325,025 cells and 49 patients) single cell multiomic dataset was generated with jointly quantified ATAC- and RNA-seq for each cell and matched genomic profiles for each patient. We identified an association between one plasma cell subtype with myeloma progression that we have called relapsed/refractory plasma cells (RRPCs). These cells are associated with 1q alterations, TP53 mutations, and higher expression of PHF19. We also identified downstream regulation of cell cycle inhibitors in these cells, possible regulation of the transcription factor (TF) PBX1 on 1q, and determined that PHF19 may be acting primarily through this subset of cells.

2024-01-31 | GSE254307 | GEO

Multiple myeloma

Project description:Multiple myeloma

| PRJNA515992 | ENA

The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma (RNA-Seq)

Project description:The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma (RNA-Seq)

| PRJNA562526 | ENA

The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma (ChIP-seq)

Project description:The role of PHF19 in promoting H3K27me3 deposition in multiple myeloma (ChIP-seq)

| PRJNA560489 | ENA

PHF19 Promotes Cell Growth and Confers Drug Resistance through EZH2 Phosphorylation in Multiple Myeloma

Project description:PHF19 Promotes Cell Growth and Confers Drug Resistance through EZH2 Phosphorylation in Multiple Myeloma