RNA sequence analysis between ECM1- sufficient and -deficient peritoneal macrophage
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ABSTRACT:
PROVIDER: PRJNA590877 | ENA |
REPOSITORIES: ENA
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Project description:We report the differential gene expression between ECM1- sufficient and -deficient peritoneal macrophage. Inflammatory bowel disease (IBD) comprises chronic relapsing disorders of the gastrointestinal tract characterized pathologically by intestinal inflammation and epithelial injury. Here, we uncover a new function of extracellular matrix protein 1 (ECM1) in promoting the pathogenesis of human and mouse IBD. ECM1 was highly expressed in macrophages, particularly tissue-infiltrated macrophages under inflammatory conditions, and ECM1 expression was significantly induced during IBD progression. The macrophage-specific knockout of ECM1 resulted in increased arginase 1 (ARG1) expression and impaired polarization into the M1 macrophage phenotype following LPS treatment.RNA-sequencing data indicated an alternative metabolic process and a higher arginine metabolic level in ECM1-deficient macrophages compared with ECM1-sufficient macrophages. A mechanistic study showed that ECM1 can negatively regulate M1 macrophage polarization through the GM-CSF/STAT5 signalling pathway. Pathological changes in mice with dextran sodium sulphate-induced IBD were alleviated by the specific knockout of the ECM1 gene in macrophages. Taken together, our findings show that ECM1 has an important function in promoting M1 macrophage polarization, which is critical for controlling inflammation and tissue repair in the intestine.
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Project description:To investigate the regulatory role of ECM1 in CCL20 expression in colorectal cancer, this study employed the human colorectal cancer SW620 cell line. Stable knockdown of ECM1 gene expression was achieved via shRNA, and single-cell transcriptome sequencing technology was used to systematically compare the transcriptomic differences between the ECM1 knockdown group (SW620-shECM1) and the negative control group (SW620-shNC). Sequencing analysis revealed that ECM1 knockdown significantly affected multiple signaling pathways, among which the TNF-α signaling pathway was notably activated, and the expression and activity of the key transcription factor JUNB underwent significant changes. Further mechanistic studies demonstrated that ECM1 regulates the transcription and expression of the downstream chemokine CCL20 by modulating the TNF-α/JUNB signaling axis. This study is the first to reveal the molecular mechanism by which ECM1 regulates CCL20 through the TNF-α-JUNB pathway in colorectal cancer at the single-cell level, providing a new perspective for understanding the role of ECM1 in the tumor microenvironment and immune regulation.
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