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

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

PROVIDER: PRJNA1149745 | ENA |

REPOSITORIES: ENA

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

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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 [TC TM]

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

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

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

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

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