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ChIP-seq analyses for KDM5A, H3K4me3, RNAPII and TAF3 in human multiple myeloma cell line MM.1S

ABSTRACT: ChIP-seq analyses for KDM5A, H3K4me3, RNAPII and TAF3 in human multiple myeloma cell line MM.1S

PROVIDER: PRJNA622960 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11476868.fastq.gz	Fastqsanger.gz
	SRR11476869.fastq.gz	Fastqsanger.gz
	SRR11476870.fastq.gz	Fastqsanger.gz
	SRR11476871.fastq.gz	Fastqsanger.gz
	SRR11476872.fastq.gz	Fastqsanger.gz

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ChIP-seq analyses for KDM5A, H3K4me3, RNAPII and TAF3 in human multiple myeloma cell line MM.1S

Project description:Recent studies have highlighted the oncogenic roles of KDM5A; however, its molecular mechanism has not been fully delineated. Here we identifies KDM5A as a transcriptional activator of MYC target genes in multiple myeloma (MM). Genetic ablation of KDM5A or pharmacologic inhibition of KDM5 by novel inhibitor JQKD82 impairs MM cell growth. Gene expression profile reveals that JQKD82 decreases expression of MYC targets. Expression of MYC targets is similarly downregulated by KDM5A depletion, but little affected by KDM5B knockdown. Mechanistically, KDM5A co-localizes with MYC across the genome, and KDM5A and MYC coordinately promote MYC target gene transcription. The treatment with JQKD82 reduces phosphorylation level of RNA polymerase II (RNAPII), resulting in RNAPII pausing, accompanied by hyper-H3K4me3 status at the MYC loci. Finally, we shows that JQKD82 exerts anti-MM activity and prolongs overall survival in vivo mouse xenograft models. Our results delineate KDM5A function that reinforces MYC transcriptional program, and identify KDM5A as a potential therapeutic target in MM.

2021-03-22 | GSE148046 | GEO

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ChIP-seq and RNA-seq analyses in human multiple myeloma cell line MM.1S

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Project description:MM.1S orthotopic tumors were analyzed fro their gene expression upon tumor outgrowth. In contorl/bortezomib/elesclmol and combo treatments.

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mRNA-sequencing for MM.1S cells that were treated with pomalidomide or were expressing shRNA against ARID2 or Aiolos.

Project description:To dissect the roles of ARID2 and Aiolos in pomalidomide-induced transcriptional changes, we performed mRNA-sequencing of MM.1S cells expressing shRNA against ARID2 or Aiolos and compared them with MM.1S cells that were treated with pomalidomide for 24, 48, or 72 hours.

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Next Generation Sequencing Facilitates Quantitative Analysis of transcriptomes in MM.1S cells treated with DMSO, All-trans retinoic acid (ATRA), carfilzomib (Cfz), and their combinations

Project description:ATRA is important for sensitizing MM cells to Cfz. To determine what signalling pathways are affected by ATRA+Cfz in MM cells, MM.1S MM cell line was pulsed with Cfz and then cultured with DMSO or 10µM ATRA for 12 h. Total RNAs of 2 x 106 MM.1S cells for each sample were extracted by RNeasy Mini Kit (Qiagen). 5-10 µg RNA samples were sent to Cancer Genomics Center at The University of Texas (Houston, TX) for genearray followed by data analysis. We use gene experssion profiling data to determine differential expression of genes in MM cells in culture with DMSO, ATRA, Cfz or ATRA+Cfz.

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Gene expression profiles of MM.1S cells after knockdown of HDAC3 or DNMT1

Project description:Previous study demonstrated that HDAC3 has a critical role in MM proliferation; however, the underlying mechanism has not yet been elucidated. We identify that HDAC3 inhibition targets DNMT1 through dual regulations. We demonstrate that knockdown of DNMT1 leads to apoptosis and significant growth inhibition in myeloma cells. HDAC3 inhibition by gene silencing or HDAC3 selective inhibitor BG45 downregulates an oncoprotein c-Myc through its acetylation. c-Myc directly regulates DNMT1 expression at its enhancer region. Furthermore, HDAC3 directly regulates the stability of DNMT1 protein through its acetylation. Pharmaceutical inhibition of HDAC3 and DNMT1 synergistically induce MM growth inhibition in in vitro and in vivo settings. The goal of this analysis is to identify genes whose expression changes after shRNA-mediated knockdown of HDAC3 or DNMT1 using the human U133 plus 2.0 Affymetrix GeneChip in myeloma cell line (MM.1S).

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