Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA918997 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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 [TC TM]

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

| PRJNA919169 | ENA

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

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

2023-08-11 | GSE222295 | GEO

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.

2017-10-31 | GSE89034 | GEO

Expression data for miR-33a over-expression in CD133-negative D456MG cells

Project description:MiR-33a is involved in the maintenance of Glioma Initiating Cells (GIC) and tumor progression. MicroRNA-33a could promote GIC growth and self-renewal by regulating two pathways including cAMP/PKA pathway and Notch pathway. We used microarrays to identify the direct target genes of miR-33a in a glioblastoma cell line D456MG. We used microarrays to detail the global change of gene expression after miR-33a over-expression and identified target genes during this process.

2014-07-17 | GSE59484 | GEO

Expression data for miR-33a over-expression in CD133-negative D456MG cells

2014-07-17 | E-GEOD-59484 | biostudies-arrayexpress

Ornithine aminotransferase supports polyamine synthesis in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDA) cells have a distinct dependence on de novo ornithine synthesis from glutamine via ornithine aminotransferase (OAT), which supports polyamine synthesis and is required for tumor growth. This directional OAT activity is normally largely restricted to infancy and contrasts with the reliance of most adult normal tissues and other cancer types on arginase (ARG) to generate arginine-derived ornithine, the substrate for polyamine synthesis. This dependence associates with arginine depletion in PDA tumor microenvironment, and is driven by mutant KRAS, which induces the expression of OAT and polyamine synthesis enzymes, including the rate-limiting enzyme ornithine decarboxylase-1 (ODC1). Loss of OAT, but not ARG2, largely mimics loss of ODC1, altering the transcriptional profiles in PDA cells, which in turn correlate with alterations in open chromatin states.

2023-01-01 | GSE193411 | GEO

mRNA expression in C-33A cells expressing HPV1 E2

Project description:Profile of RNA expression in a C-33A cell line derived from an HPV negative cervical carcinoma in the presence or absence of HPV1 E2 expression. mRNA profiles of C-33A cells in presence or absence of HPV1 E2 expression were generated by deep sequencing using Illumina GAIIx. Two samples (no replicates). One control and one experimental.

2014-04-14 | E-GEOD-52367 | biostudies-arrayexpress

mRNA expression in C-33A cells expressing HPV1 E2

Project description:Profile of RNA expression in a C-33A cell line derived from an HPV negative cervical carcinoma in the presence or absence of HPV1 E2 expression.

2014-04-14 | GSE52367 | GEO

Enterobacter cloacae BIDMC 33A

Project description:Enterobacter cloacae BIDMC 33A Genome sequencing and assembly

| PRJNA202044 | ENA