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).
2019-08-31 | GSE136665 | GEO
Project description:The aim was to look for target genes of miR-15a-5p or miR-21-5p.
2021-02-11 | E-MTAB-8776 | biostudies-arrayexpress
Project description:Gene expression analysis of stable HMGA2-overexpressing DLD-1 cells (DLD-1-HMGA2) and its control cells (DLD-1-Vector).
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Project description:Preimplantation embryos cultured in vitro exhibit increased stress and apoptosis compared with in vivo development. miR-21-5p is a conserved, highly abundant microRNA in reproductive-tract extracellular vesicles and has been implicated in cell-survival pathways. To define its transcriptomic impact on early embryos, we performed RNA-seq on mouse blastocysts generated by IVF and cultured in KSOM with either miR-21-5p agomir (50 nM) or blank control. Each biological replicate consisted of five pooled blastocysts; n=4 replicates per group. Sequencing was carried out on an Illumina NovaSeq X Plus.
2026-06-15 | GSE308541 | GEO
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:Regular exercise before stroke has been associated with reduced neurological injury after ischemic stroke; however, its effects on microvascular remodeling in the ischemic penumbra and the underlying molecular mechanisms remain incompletely understood. In this study, a rat middle cerebral artery occlusion/reperfusion (MCAO/R) model was established. Rats underwent 3 weeks of moderate-intensity aerobic exercise preconditioning, and its effects on neurological deficits, cerebral infarct volume, TUNEL-positive cell death, and microvascular remodeling after cerebral ischemia/reperfusion injury (CIRI) were evaluated. The underlying mechanisms were investigated using integrated transcriptomic analysis and targeted molecular validation. Exercise preconditioning alleviated neurological deficits, reduced cerebral infarct volume and TUNEL-positive cell death, increased CD31-positive vascular coverage and vascular length, and enhanced the expression of endothelial junction-associated proteins, including ZO-1 and VE-cadherin. Integrated miRNA-mRNA transcriptomic analysis identified the miR-21-5p/RasGRP1/Ras/ERK signaling axis as a candidate pathway underlying the neurovascular protective effects of exercise preconditioning. Further validation demonstrated that exercise preconditioning reduced miR-21-5p expression, increased RasGRP1 expression, and enhanced Ras/ERK signaling activity. Conversely, miR-21-5p overexpression or RasGRP1 knockdown attenuated the beneficial effects of exercise preconditioning on neurological deficits, tissue injury, and microvascular remodeling. These findings suggest that exercise preconditioning promotes early neurovascular protection after CIRI, at least partly through modulation of the miR-21-5p/RasGRP1/Ras/ERK signaling axis, providing new insights into exercise-mediated stroke protection and potential therapeutic targets.
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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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