MiR-21-5p-driven gene expression in human colorectal DLD-1 cells.
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ABSTRACT:
PROVIDER: PRJNA563004 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression analysis of stable miR-21-5p-overexpressing DLD-1 cells (DLD-1-miR-21) and its control cells (DLD-1-miR-Vec).
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Project description:Aims This study investigated the impact of hepatocyte exosomes on hepatic stellate cell (HSC) activation and their potential role in liver fibrosis while elucidating the underlying molecular mechanisms. Methods L02 exosomes were extracted, and their influence on LX-2 activation was preliminarily investigated. A mouse liver fibrosis model was established through intraperitoneal injection of 20% carbon tetrachloride (CCl4). Normal and fibrotic hepatocyte exosomes were separately collected to explore their distinct effects on HSC activation. High-throughput sequencing identified differential miRNAs in exosomes from normal and fibrotic hepatocytes. MiR-21-5p, displaying the most substantial expression difference, was selected to assess the correlation between serum exosomal miR-21-5p and liver fibrosis. The target gene of miR-21-5p was validated using a dual luciferase assay. LX-2 cells were transfected with miR-21-5p mimics and inhibitors to clarify the impact and mechanisms of miR-21-5p on HSC activation, proliferation, and collagen synthesis. Results Normal L02 exosomes were internalized by LX-2 cells and inhibited their activation. In comparison to normal hepatocyte exosomes, fibrotic hepatocyte exosomes induced HSC activation. High-throughput sequencing revealed 32 upregulated and 6 downregulated miRNAs in fibrotic hepatocyte exosomes, with the most significant increase observed in miR-21-5p. Serum exosomal miR-21-5p displayed a close association with liver fibrosis. Dual luciferase assays and cell transfection experiments confirmed that miR-21-5p promoted HSC activation, proliferation, and collagen synthesis by targeting Smad7. Conclusion Fibrotic hepatocyte exosomes may trigger HSCs activation through exosomal transfer in liver fibrosis. Exosomal miR-21-5p enhances HSCs activation, proliferation, and collagen synthesis by targeting Smad7, potentially serving as a diagnostic marker and therapeutic target for liver fibrosis.
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Project description:HMGA2-driven gene expression in human colorectal DLD-1 cells.
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Project description:Meningiomas are common intracranial tumors. Most of thenm benign WHO GI tumors, while approximately 20% are diagnosed as progressively more aggressive GII and GIII meningiomas. The study aimed to identify genes with tumor grade-related expression and to assess their functional relevance. The effect of selected miRNAs including hsa-miR-21-5p and hsa-miR-1265 on the cell phenotypep and genes expression profile was investigated using in vitro culturing of menignigioma cells KT21-MG1 andd Ben-Men-1. The cells were cultured with specific synthetic miRNA (miRNA mimic) or or nonspeciic control miRNA. Genes expression in miRNA-treated anad control cells was determined with RNAseq.
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Project description:Marked heterogeneity in radiosensitivity is a major challenge in the treatment of oral squamous cell carcinoma (OSCC), often resulting in poor outcomes for radioresistant tumors. The underlying molecular drivers of this resistance remain elusive. Here, we identify a novel mechanism in which miR-21-5p promotes radiation resistance by selectively activating the error-prone DNA double-strand break (DSB) repair pathway alternative end-joining (Alt-EJ). Integrative miRNA profiling, multi-omic analyses, and functional assays demonstrate that miR-21-5p upregulation coupled with suppression of its target gene signature increases Alt-EJ dependence for DSB repair. This Alt-EJ reliance enhances genomic instability, increases tumor mutational burden and microhomology-mediated indels, and confers pronounced radiation resistance in OSCC models, while correlating with poor radiotherapy response in patients. Importantly, pharmacological or genetic inhibition of Alt-EJ components, including PARP1 and POLQ, restores radiosensitivity in vitro and in vivo, with PARP1 inhibition specifically reversing miR-21-5p-mediated resistance in a syngeneic mouse model. Further RNA-seq analyses of these mice tumors confirmed that PARP inhibitor induced selective radiosensitization effects for miR-21-5p-overexpressing tumors were accompanied by a pronounced reduction in alt-EJ expression. Collectively, these findings establish the miR-21-5p/Alt-EJ axis as a key driver of radiation resistance in OSCC and support Alt-EJ targeting as a promising approach for precision radiosensitization.
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Project description:In order to comprehensively identify genes directly regulated by AP4, a genome-wide chromatin-immunoprecipitation analysis (ChIP) followed by next generation sequencing (ChIP-seq) was performed after activation of a conditional AP4 allele in DLD-1 cells. One DLD-1 Sample was sequenced.
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