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Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [TC TM]

ABSTRACT: Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [TC TM]

PROVIDER: PRJNA919169 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22997500_1.fastq.gz	Fastqsanger.gz
	SRR22997500_2.fastq.gz	Fastqsanger.gz
	SRR22997501_1.fastq.gz	Fastqsanger.gz
	SRR22997501_2.fastq.gz	Fastqsanger.gz
	SRR22997502_1.fastq.gz	Fastqsanger.gz

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Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [TC TM]

Project description:Breast cancer cells secret different kinds of cargoes through extracellular vesicles (EVs) especially under stress conditions. However, the underling mechanism and function is poorly defined. Here, we found RNA binding protein ACO1 could bind miR-33a and assist their package into EVs in tumor core region. Thereby, miR-33a suppressed putrescine metabolism in cancer-associated fibroblasts (CAFs) and reprogrammed H3K4me3 mediated epigenetic regulation. Chip-seq data suggested stress granules related genes were downregulated and ECM related genes were upregulated. Most notably, putrescine inhibited KDM5C expression level but did not altered activity. Finally, our study provides a novel mechanism of how cancer EVs reprogrammed polyamine metabolism in tumor stroma, leading to spatially different distribution of ECM in tumor microenvironment.

2023-08-09 | GSE222291 | GEO

Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [miRNA-Seq]

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Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [CAF EV]

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Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism

Project description:Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism

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Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [CAF EV]

Project description:Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [CAF EV]

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Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [miRNA-Seq]

Project description:Starvation induced circulating miR-33a secretion remodeled extracellular matrix of tumor microenvironment by altering polyamine metabolism [miRNA-Seq]

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Cancer-cell-secreted miR-33a remodels extracellular matrix by targeting polyamine metabolism in stroma to promote tumorigenesis

Project description:Tumor progression depends on the bidirectional interactions between cancer and stroma in the heterogenous tumor microenvironment (TME) partially through extracellular vesicles (EVs). However, the secretary mechanism and biological effect of cancer cell derived EVs on tumor survival under starvation is poorly defined. Here, we identify cancer cells preferentially secrete miR-33a in the tumor core region with poor nutrient level. Exosomal miR-33a suppresses putrescine biosynthesis by targeting AGMAT in stromal cells, where putrescine suppresses the expression of demethylase KDM5C. Chromatin immunoprecipitation sequencing identifies miR-33a/KDM5C axis tightly regulates TIA1 gene, functioning stress granule (SG) marker. Exosomal miR-33a diminishes the assembly of stromal SGs but inducing more extracellular matrix accumulation. Collectively, our study reveals tumor selectively secretes miR-33a through EVs to remodel the stromal SG formation and extracellular matrix profiles to gain survival possibility for cancer cells under starvation, highlighting a novel regulatory mechanism of nutrient level on EV secretion and the function of polyamine metabolism in reshaping epigenetic profiles of TME.

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Iron reshapes polyamine metabolism through controlling exosomal miR-33a secretion to remodel extracellular matrix in tumor microenvironment

Project description:Tumor progression depends on the bidirectional interactions between cancer and stroma in the heterogenous tumor microenvironment (TME) partially through extracellular vesicles (EVs). However, the secretion mechanism and biological effect of cancer cell-derived EVs on tumor survival under starvation is poorly defined. Here, we demonstrate cancer cells selectively secrete miR-33a with the assistance of protein ACO1 under glucose starvation and lower iron level, which affiliates the binding capability of miR-33a and ACO1. Exosomal miR-33 suppresses putrescine biosynthesis by targeting AGMAT in tumor stroma, where putrescine inhibits the expression of demethylase KDM5C. TIA1 gene, stress granule (SG) marker, is tightly regulated by miR-33a/KDM5C axis. Exosomal miR-33a diminishes the formation of SGs in tumor stroma but inducing more fibronectin secretion into TME. Collectively, our study reveals tumor secrets distinct EV cargoes to remodel the SGs and extracellular matrix of TME to gain survival possibility, highlighting a novel regulatory mechanism of iron and nutrient level on EV secretion in TME.

2025-09-10 | GSE241351 | GEO

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Gene expression profiling in prostate cancer cell lines transfected with miR-33a

Project description:In this study, we aimed to investigate the functional roles of miR-33a in PCa.We investigated the relative miR-33a level in normal and tumor prostate samples as well as PCa cell lines. Then, we performed a detailed functional analysis of mir-33a in LNCaP and VCaP PCa cells and evaluated proliferative, invasive and anchorage independent growth potential of cells upon overexpression and knockdown of miR-33a. We next explored the potential direct targets of miR-33a in PCa cells via utilizing gene expression microarray analysis, bioinformatics search, further qRT-PCR, western blot, and luciferase assay confirmation. Our results demonstrated that miR-33a is significantly downregulated in PCa tumor samples and PCa cell lines, pointing its tumor suppressor potential in PCa. Overexpression and knockdown of miR-33a significantly altered the proliferative, invasive and anchorage independent growth potentials of cells through altering the expression of its direct target PIM1. Ectopic induction of MiR-33a expression reversed the impacts of PIM1 overexpression on cellular phenotypes associated with PCa progression. Our results suggest that mir-33a exerts its tumor suppressor potential through targeting its direct target PIM1 and carries crucial roles in PCa tumorigenesis.

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