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The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE75743 | GEO | 2017/12/31

SECONDARY ACCESSION(S): PRJNA305256

REPOSITORIES: GEO

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The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis [RNA-Seq_HPTB]

Project description:Comprehensive RNA-seq experiments in DMSO and HPTB (inhibitor of PRMT5) treated cells delineate the role of PRMT5 complex in promoting breast cancer oncogenesis

2017-12-31 | GSE75742 | GEO

The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis [RNA-Seq]

Project description:Comprehensive RNA-seq experiments in control and PRMT5 and WDR77 shRNA infected cells delineate the role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis

2017-12-31 | GSE75741 | GEO

The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis [ChIP-Seq]

Project description:The PRMT5/WDR77 complex is known to regulate alternative splicing through the symmetric dimethylation of spliceosome proteins in the cytoplasm. Overexpression of this complex is observed in different types of cancer including breast cancer, where it shows increased nuclear accumulation.To understand the nuclear role and the chromatin binding properties of PRMT5 we performed genome-wide ChIP-Seq analysis in the breast cancer cell line MDA-MB-231.

2017-12-31 | GSE75739 | GEO

The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis

Project description:The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis

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The PRMT5/WDR77 complex regulates alternative splicing through ZNF326 in breast cancer.

Project description:We observed overexpression and increased intra-nuclear accumulation of the PRMT5/WDR77 in breast cancer cell lines relative to immortalized breast epithelial cells. Utilizing mass spectrometry and biochemistry approaches we identified the Zn-finger protein ZNF326, as a novel interaction partner and substrate of the nuclear PRMT5/WDR77 complex. ZNF326 is symmetrically dimethylated at arginine 175 (R175) and this modification is lost in a PRMT5 and WDR77-dependent manner. Loss of PRMT5 or WDR77 in MDA-MB-231 cells leads to defects in alternative splicing, including inclusion of A-T rich exons in target genes, a phenomenon that has previously been observed upon loss of ZNF326. We observed that the alternatively spliced transcripts of a subset of these genes, involved in proliferation and tumor cell migration like REPIN1/AP4, ST3GAL6, TRNAU1AP and PFKM are degraded upon loss of PRMT5. In summary, we have identified a novel mechanism through which the PRMT5/WDR77 complex maintains the balance between splicing and mRNA stability through methylation of ZNF326.

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The PRMT5/WDR77 complex restricts hepatitis E virus replication.

Project description:Hepatitis E virus (HEV) is one of the main pathogenic agents of acute hepatitis in the world. The mechanism of HEV replication, especially host factors governing HEV replication is still not clear. Here, using HEV ORF1 trans-complementation cell culture system and HEV replicon system, combining with stable isotope labelling with amino acids in cell culture (SILAC) and mass spectrometry (MS), we aimed to identify the host factors regulating HEV replication. We identified a diversity of host factors associated with HEV ORF1 protein, which were putatively responsible for viral genomic RNA replication, in these two cell culture models. Of note, the protein arginine methyltransferase 5 (PRMT5)/WDR77 complex was identified in both cell culture models as the top hit. Furthermore, we demonstrated that PRMT5 and WDR77 can specifically inhibit HEV replication, but not other viruses such as HCV or SARS-CoV-2, and this inhibition is conserved among different HEV strains and genotypes. Mechanistically, PRMT5/WDR77 can catalyse methylation of ORF1 on its R458, impairing its replicase activity, and virus bearing R458K mutation in ORF1 relieves the restriction of PRMT5/WDR77 accordingly. Taken together, our study promotes more comprehensive understanding of viral infections but also provides therapeutic targets for intervention.

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TBL2 Promotes Tumorigenesis via PRMT5/WDR77-Mediated AKT Activation in Breast Cancer.

Project description:Breast cancer (BC) is a common malignancy that affects women worldwide. Although transducing beta-like 2 (TBL2), a member of the WD40 repeat protein family, has been implicated in various intracellular signaling pathways, its precise function in BC remains unclear. The expression of TBL2 is analyzed using real-time PCR, western blotting, and immunohistochemistry in BC patient specimens. Kaplan-Meier survival analysis is employed to assess its prognostic significance. Proteomic analysis, immunoprecipitation tests, and protein immunoblotting are employed to examine the impact of TBL2 on AKT phosphorylation activation. The findings reveal selective overexpression of TBL2 in BC, correlating significantly with various clinicopathological characteristics and poor survival outcomes in patients with BC. Through in vivo and in vitro experiments, it is observed that TBL2 suppression inhibits BC cell proliferation, while TBL2 overexpression has the opposite effect. Mechanistically, TBL2 is identified as a scaffolding protein that promotes PRMT5 and WDR77 interaction. This interaction enhances the methyltransferase activity of PRMT5, leading to increased AKT phosphorylation activation and promotion of breast cancer cell proliferation. In conclusion, this study uncovers a novel function of TBL2 in the activation of AKT by PRMT5 and suggests TBL2 as a potential therapeutic target for BC treatment.

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