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Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (scATAC-Seq)

ABSTRACT: Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (scATAC-Seq)

PROVIDER: PRJNA852958 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19854516_1.fastq.gz	Fastqsanger.gz
	SRR19854516_2.fastq.gz	Fastqsanger.gz
	SRR19854517_1.fastq.gz	Fastqsanger.gz
	SRR19854517_2.fastq.gz	Fastqsanger.gz
	SRR19854518_1.fastq.gz	Fastqsanger.gz

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Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance (scATAC-Seq)

Project description:Targeted monoclonal antibody therapy has emerged as a powerful therapeutic strategy for cancer. Unfortunately, only a minority of patients haves durable responses and the development of resistance remains a major clinical obstacle. Antibody-dependent cell-mediated cytotoxicity (ADCC) represents a crucial therapeutic mechanism of action; however few studies have explored ADCC resistance. Using multiple in vitro models of ADCC selection pressure, we have uncovered both shared and distinct resistance mechanisms. We employed CITE sequencing and single-cell ATAC-seqeuncing to interrogate molecular mechanisms of resistance.

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Project description:Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance

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Antibody Dependent Cell-Mediated Cytotoxicity Selection Pressure Induces Diverse Mechanisms of Resistance

Project description:This SuperSeries is composed of the SubSeries listed below.

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Antibody dependent cell-mediated cytotoxicity selection pressure induces diverse mechanisms of resistance.

Project description:Targeted monoclonal antibody therapy has emerged as a powerful therapeutic strategy for cancer. However, only a minority of patients have durable responses and the development of resistance remains a major clinical obstacle. Antibody-dependent cell-mediated cytotoxicity (ADCC) represents a crucial therapeutic mechanism of action; however, few studies have explored ADCC resistance. Using multiple in vitro models of ADCC selection pressure, we have uncovered both shared and distinct resistance mechanisms. Persistent ADCC selection pressure yielded ADCC-resistant cells that are characterized by a loss of NK cell conjugation and this shared resistance phenotype is associated with cell-line dependent modulation of cell surface proteins that contribute to immune synapse formation and NK cell function. We employed single-cell RNA sequencing and proteomic screens to interrogate molecular mechanisms of resistance. We demonstrate that ADCC resistance involves upregulation of interferon/STAT1 and DNA damage response signaling as well as activation of the immunoproteasome. Here, we identify pathways that modulate ADCC sensitivity and report strategies to enhance ADCC-mediated elimination of cancer cells. ADCC resistance could not be reversed with combinatorial treatment approaches. Hence, our findings indicate that tumor cells utilize multiple strategies to inhibit NK cell mediated-ADCC. Future research and development of NK cell-based immunotherapies must incorporate plans to address or potentially prevent the induction of resistance.

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