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Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 2]

ABSTRACT: Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 2]

PROVIDER: PRJNA951450 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24044131.fastq.gz	Fastqsanger.gz
	SRR24044132.fastq.gz	Fastqsanger.gz
	SRR24044133.fastq.gz	Fastqsanger.gz

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Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 1]

Project description:Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 1]

| PRJNA951448 | ENA

Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 1]

Project description:Anti-CD38 monoclonal antibodies like Daratumumab (Dara) are effective in multiple myeloma (MM); however, drug resistance ultimately occurs and the mechanisms behind this are poorly understood. Here, we performed two in vitro genome-wide CRISPR screens to systematically discover the regulators of sensitivity to Dara-mediated antibody-dependent cellular cytotoxicity (ADCC) and identified KDM6A. The loss of KDM6A led to a marked downregulation in CD38 expression by increasing H3K27me3 on the CD38 promoter, resulting in resistance to Dara-mediated ADCC. Yet, adding back CD38 did not completely rescue this phenotype. In fact, KDM6A loss also downregulated CD48, which promoted Dara resistance by inhibiting natural killer cell activity. Lowering the H3K27me3 with an EZH2 inhibitor restored sensitivity to Dara through CD38 and CD48 upregulation. These findings suggest KDM6A loss as a mechanism of Dara resistance and explore the strategy of using an EZH2 inhibitor, one of which is already FDA-approved, to improve the response to Dara in MM.

2024-01-23 | GSE228767 | GEO

Epigenetic regulation of NK cell-mediated immune response in multiple myeloma [CRISPR screening 2]

2024-01-23 | GSE228770 | GEO

Multiple myeloma

Project description:Multiple myeloma

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Surfaceome CRISPR activation screening uncovers ligands regulating tumor sensitivity to NK cell killing

Project description:Natural killer (NK) cell-based immunotherapies represent a promising avenue for cancer treatment due to their ability to eliminate cancer cells independently of antigen presentation and potential for “off-the-shelf” use. However, the molecular determinants governing tumor cell susceptibility to NK cell-mediated cytotoxicity remain incompletely understood. Here we employed CRISPR activation (CRISPRa) screening to systematically identify cancer cell surface regulators of NK cell killing across multiple cancer types. Using a comprehensive surfaceome-focused library, we screened human and murine cancer cell lines co-cultured with NK cells, identifying both known and novel ligands that modulate NK cell cytotoxicity. Our screens revealed established factors including CD43 (encoded by SPN), while uncovering previously uncharacterized regulators such as CD44, PDPN, and Siglec-1/CD169. Validation through complementary cDNA overexpression and genetic knockout approaches confirmed that disruption of CD43, CD44, PDPN, and Siglec-1 significantly altered cancer cell susceptibility to NK killing both in vitro and in humanized mouse models. Analysis of clinical datasets show that expression of identified factors correlates with patient survival outcomes in an NK-context dependent manner supporting their therapeutic relevance. Most notably, our mechanistic studies demonstrate that CD43-mediated NK cell resistance operates independently of its previously proposed interaction with Siglec-7 on NK cells. Furthermore, we find that targeting CD43 on either NK cells or engineered T cells substantially enhances their cytotoxic activity against leukemia cell lines. These results establish gain-of-function screening as a powerful approach for discovering immunoregulatory surface proteins and identify multiple promising targets for enhancing NK cell-based cancer immunotherapies.

2026-04-15 | GSE327341 | GEO

Genome-wide screening of FOXM1 expression in multiple myeloma cells

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Genome-wide screening of IKZF1 binding in multiple myeloma cells.

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Genome-wide CRISPR-Cas9 knockout screening identifies NUDCD2 depletion as sensitizer for bortezomib, carfilzomib and ixazomib in multiple myeloma [CRISPR screen carfilzomib]

Project description:Genome-wide CRISPR-Cas9 knockout screening identifies NUDCD2 depletion as sensitizer for bortezomib, carfilzomib and ixazomib in multiple myeloma [CRISPR screen carfilzomib]

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Genome-wide CRISPR-Cas9 knockout screening identifies NUDCD2 depletion as sensitizer for bortezomib, carfilzomib and ixazomib in multiple myeloma [CRISPR screen bortezomib]

Project description:Genome-wide CRISPR-Cas9 knockout screening identifies NUDCD2 depletion as sensitizer for bortezomib, carfilzomib and ixazomib in multiple myeloma [CRISPR screen bortezomib]

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