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Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [scRNAseq]

ABSTRACT: Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [scRNAseq]

PROVIDER: PRJNA1089539 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28386576_1.fastq.gz	Fastqsanger.gz
	SRR28386576_2.fastq.gz	Fastqsanger.gz
	SRR28386577_1.fastq.gz	Fastqsanger.gz
	SRR28386577_2.fastq.gz	Fastqsanger.gz
	SRR28386578_1.fastq.gz	Fastqsanger.gz

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Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [scRNAseq]

Project description:Drug resistance is the principal challenge of cancer therapies, including recently developed immunotherapy. More and more popular use of immunotherapy, especially treatments with immune checkpoint inhibitors (ICIs), witnesses explosively increasing cases of both primary and acquired immunotherapy resistance. While primary resistance has been extensively studied, mechanisms underlying acquired resistance of immunotherapy are less understood. Here we reported that tumor cells could develop acquired resistance to ICI treatment through self-built collagen-containing physical barriers in non-small cell lung cancer (NSCLC). We found that tumor cells expressed high levels of multiple collagen genes, including COL3A1 and COL6A1, and were fully covered with collagen fibers. COL3A1 formed a castle-like structure of a cluster of tumor cells and prevented the infiltration of T cells, while COL6A1 seemed to be an armor-like structure of each tumor cell and protected them from attack by cytotoxic T cells. Genetic or pharmaceutic disruption of these collagens, by warfarin, a commonly used medicine, significantly reversed the acquired resistance. Thus, our data reveal an unprecedented tumor cell-intrinsic mechanism, mediated by collagen-containing physical barriers, of acquired immunotherapy resistance, which immediately suggests a treatment option for patients.

2025-02-01 | GSE261898 | GEO

Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [spatial]

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Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [bulk RNAseq]

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Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [spatial]

Project description:Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [spatial]

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Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [bulk RNAseq]

Project description:Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [bulk RNAseq]

| PRJNA1089513 | ENA

scRNAseq of longitidunally acquired samples from a CLL patient

Project description:scRNAseq of longitidunally acquired samples from a CLL patient

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scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [1]

Project description:Serial blood draws from a single patient and serial tumor biopsies from the same patient with metastatic Merkel cell polyomavirus Merkel cell carcinoma, who was treated with cellular immunotherapy targeting MCPyV (autologous endogenous T cell therapy) followed by checkpoint inhibitors (anti-PD1 and anti-CTLA4). The patient had a 22 month clinical response followed by late/acquired resistance. We performed scRNAseq using the 10x genomics 3' Chromium expression assay to determine potential mechanisms contributing to immunotherapy response and late resistance

2018-09-01 | GSE117988 | GEO

scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [1]

Project description:scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [1]

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scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [2]

Project description:scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [2]

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MCM complexes are barriers that restrict loops and TADs

Project description:Eukaryotic genomes are compacted into loops and topologically associating domains (TADs), which contribute to transcription, recombination and genomic stability. Cohesin extrudes DNA into loops that are thought to lengthen until it encounters CTCF boundaries. Little is known whether loop extrusion is impeded by macromolecular machines. We demonstrate that the replicative helicase MCM is a barrier that restricts loops and TADs in G1 phase. Single-nucleus Hi-C of one-cell embryos revealed that MCM loading reduces CTCF-anchored loops and increases TAD boundary insulation, suggesting loop extrusion is impeded before reaching CTCF. Single-molecule imaging provides evidence that MCM are physical barriers that constrain cohesin translocation in vitro. Simulations are consistent with MCM as abundant, random barriers with low permeability. We conclude that distinct loop extrusion barriers contribute to shaping 3D genomes.

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