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SMARCA4 reads PRMT1-mediated H4R3me2a to promote colorectal cancer progression I

ABSTRACT: SMARCA4 reads PRMT1-mediated H4R3me2a to promote colorectal cancer progression I

PROVIDER: PRJNA599181 | ENA |

REPOSITORIES: ENA

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SMARCA4 reads PRMT1-mediated H4R3me2a to promote colorectal cancer progression II

Project description:To further investigate the functional associations between PRMT1 and SMARCA4 and explore the biological significance of these interactions, we conducted expression profiling on the Agilent SurePrint G3 Human Gene Expression v3 (8*60K,Design ID:072363) using knockdown of PRMT1 or SMARCA4’s RNA in HCT116 cells.

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SMARCA4 reads PRMT1-mediated H4R3me2a to promote colorectal cancer progression I

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SMARCA4 reads PRMT1-mediated H4R3me2a to promote colorectal cancer progression II

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PRMT1-mediated H4R3me2a recruits SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling.

Project description: Not available

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Correction to: PRMT1-mediated H4R3me2a recruits SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling.

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WNT-driven PRMT1 Nuclear Localization Generates Synthetic Lethality in Colorectal Cancers

Project description:Colorectal cancer (CRC) arises from multi-step accumulation of genetic and epigenetic mutations that deregulate intestinal homeostasis leading to neoplastic transformation and metastases. Constitutive activation of WNT signaling is considered the initial driver oncogenic event to which CRCs remain addicted, also in their most aggressive metastatic forms. WNT activation provokes an aberrant signaling that converges into the nucleus where transcription and chromatin-remodeling factors cooperate to regulate cell identity. This leads to deregulated proliferation, block of differentiation and evasion from cell death pathways. We found that the protein arginine methyltransferase 1 (PRMT1) is synthetic lethal with WNT oncogenic activation in both genetically-defined mouse models and patient-derived metastatic CRC organoids. WNT activation regulates the subcellular localization of PRMT1, inducing its complete nuclear translocation. This makes CRCs specifically dependent on PRMT1 enzymatic activity to sustain WNT-dependent proliferation regardless of the mutational landscape carried by distinct patients. Together these data uncover a new molecular crosstalk between WNT activation and PRMT1 activity and place PRMT1 inhibition as a potential strategy to counteract CRC addiction to WNT oncogenic activation.

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ACTB methylation regulates SMARCA4 genomic occupancy to promote translation and reduce adhesion in colorectal cancer cells

Project description:ACTB is a cytoskeletal protein involved in intracellular trafficking. In recent years, it has become evident that, in addition to its established roles in these compartments, ACTB also participates in the regulation of transcription. However, the molecular mechanisms underlying this function remain poorly understood. The methyltransferase SETD3 has previously been shown to methylate ACTB at H73, thereby regulating ACTB polymerization and smooth muscle contraction. Here, we show that the genomic distribution of ACTB is SETD3-dependent and that this regulation modulates the transcription of genes involved in cell adhesion and mRNA translation in colorectal cancer cells. Proteomic analyses reveal that ACTB and SETD3 interact with multiple large protein complexes, including complexes associated with transcriptional regulation. Specifically, we demonstrate that SETD3-mediated ACTB methylation is required for the co-localization of SMARCA4, a subunit of the SWI/SNF BAF complex, at specific genomic loci. Genomic analyses further show that this co-localization enables the coordinated occupancy of SMARCA4 and H73-methylated ACTB at genes involved in cell adhesion and mRNA translation. Finally, phenotypic assays confirm these regulatory effects. Together, these findings uncover a new mechanistic layer of selective transcriptional regulation mediated by an ACTB–SETD3–SMARCA4 axis in colorectal cancer cells.

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Project description:ACTB methylation regulates SMARCA4 genomic occupancy to promote translation and reduce adhesion in colorectal cancer cells

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Project description:ACTB methylation regulates SMARCA4 genomic occupancy to promote translation and reduce adhesion in colorectal cancer cells

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