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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 promotes growth of pediatric high grade glioma [ChIP-seq]

Project description:Background. Pediatric high-grade gliomas (PHGG) are aggressive, undifferentiated CNS tumors with poor outcomes, for which no standard-of-care drug therapy currently exists. Through a knockdown screen for epigenetic regulators, we identified PRMT5 as essential for PHGG cell growth. We hypothesized that, similar to its effect in normal cells, PRMT5 promotes self-renewal of stem-like PHGG tumor initiating cells (TICs) essential for tumor growth. Methods. We conducted in vitro analyses, including limiting dilution studies of self-renewal, to determine the phenotypic effects of PRMT5 KD. We performed ChIP-Seq to identify PRMT5-mediated epigenetic changes and gene set enrichment analysis to identify pathways that PRMT5 regulates. Using an orthotopic xenograft model of PHGG, we tracked survival and histological characteristics resulting from PRMT5 KD or administration of a PRMT5 inhibitor ± radiation therapy (RT). Results. In vitro, PRMT5 KD slowed cell cycle progression, tumor growth and self-renewal. PRMT5 KD reduced H3K4me3 occupancy at genes associated with self-renewal, tumor formation and growth. In vivo, PRMT5 KD increased survival and reduced tumor aggressiveness; however, pharmacological inhibition of PRMT5 with or without RT did not improve survival. Conclusion. PRMT5 KD epigenetically reduced TIC self-renewal, leading to increased survival in preclinical models. Pharmacological inhibition of PRMT5 enzymatic activity may have failed in vivo due to insufficient reduction of PRMT5 activity by chemical inhibition, or this failure may suggest that non-enzymatic activities of PRMT5 are more relevant.

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

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