Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA217455 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs are epigenetic regulators of T cell maturation and exhaustion. However, the specific mechanisms by which miRNAs modulate T cell functions during tumor development are not well understood. Here, we demonstrate that miR-379-5p counteracts the exhaustion phenotype induced by chronic T cell stimulation, enhancing anti-tumor effector functions. MiR-379-5p is downregulated in exhausted T cells, negatively associated with exhausted tumor-infiltrating lymphocytes in advanced tumors, and positively correlated with favorable survival in breast cancer and other cancer types. MiR-379-5p directly targets the 3' untranslated region (3’-UTR) of TIM3 and TIGIT, suppressing their expression in CD8 T cells. Ectopic miR-379-5p expression directs differentiation to memory-like effector cells, enhancing cancer cell killing activity. Conversely, the nuclear receptor NR4A1 negatively regulates miR-379 in T cells, restoring immune checkpoint gene expression and mitigating the cancer-killing ability. OT-1 T cells expressing miR-379-5p have elevated cytotoxic killing against B16F10-OVA tumors in NOD-SCID mice. Importantly, autologous T cells isolated from breast cancer patients introduced with miR-379-5p significantly increase their killing activity against tumor organoids derived from the matched patients. Our findings identify miR-379-5p as an epigenetic tumor suppressor that promotes CD8+ T cell effector functions, offering promise for novel cancer immunotherapy strategies.
2025-04-23 | GSE271248 | GEO
Project description:Natural and synthetic circular RNAs effectively impair miRNA function. MiR-21-5p is a potent oncomiR presenting ~33% of all miRNAs across cancers, ~41% in lung adenocarcinoma (LUAD), and ~68% in LUAD-derived cells. We validate and identify five main tumor suppressors targeted by miR-21-5p by deletion of the MIR21 locus in LUAD cells. Synthetic, liposome-delivered circular miR-21-5p decoys enhance expression of these tumor suppressors and severely impair tumor cell vitality at low doses. Decoy efficacy is not increased by bulging of miR-21-5p targeting sites, but associated with substantial cellular decoy stability, indicated by a half-life of ~20h. The intraperitoneal application of nanoparticle-delivered miR-21-5p decoys significantly impairs tumor growth in mouse LUAD tumor models. Decoys are well tolerated and were enriched in lung tissue. However, despite low decoy abundance, tumor suppressor expression was only increased in subcutaneous tumors. These findings suggest nanoparticle-delivered circular miRNA decoys as potent therapeutics in cancer treatment.
2020-07-20 | GSE148735 | GEO
Project description:Natural and synthetic circular RNAs effectively impair miRNA function. MiR-21-5p is a potent oncomiR presenting ~33% of all miRNAs across cancers, ~41% in lung adenocarcinoma (LUAD), and ~68% in LUAD-derived cells. We validate and identify five main tumor suppressors targeted by miR-21-5p by deletion of the MIR21 locus in LUAD cells. Synthetic, liposome-delivered circular miR-21-5p decoys enhance expression of these tumor suppressors and severely impair tumor cell vitality at low doses. Decoy efficacy is not increased by bulging of miR-21-5p targeting sites, but associated with substantial cellular decoy stability, indicated by a half-life of ~20h. The intraperitoneal application of nanoparticle-delivered miR-21-5p decoys significantly impairs tumor growth in mouse LUAD tumor models. Decoys are well tolerated and were enriched in lung tissue. However, despite low decoy abundance, tumor suppressor expression was only increased in subcutaneous tumors. These findings suggest nanoparticle-delivered circular miRNA decoys as potent therapeutics in cancer treatment.
2020-07-20 | GSE148734 | GEO
Project description:Natural and synthetic circular RNAs effectively impair miRNA function. MiR-21-5p is a potent oncomiR presenting ~33% of all miRNAs across cancers, ~41% in lung adenocarcinoma (LUAD), and ~68% in LUAD-derived cells. We validate and identify five main tumor suppressors targeted by miR-21-5p by deletion of the MIR21 locus in LUAD cells. Synthetic, liposome-delivered circular miR-21-5p decoys enhance expression of these tumor suppressors and severely impair tumor cell vitality at low doses. Decoy efficacy is not increased by bulging of miR-21-5p targeting sites, but associated with substantial cellular decoy stability, indicated by a half-life of ~20h. The intraperitoneal application of nanoparticle-delivered miR-21-5p decoys significantly impairs tumor growth in mouse LUAD tumor models. Decoys are well tolerated and were enriched in lung tissue. However, despite low decoy abundance, tumor suppressor expression was only increased in subcutaneous tumors. These findings suggest nanoparticle-delivered circular miRNA decoys as potent therapeutics in cancer treatment.
2020-07-20 | GSE148684 | GEO
Project description:Inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene is one of the first truncal event in clear cell Renal Cell Carcinoma (ccRCC) tumorigenesis. Accumulation of the Hypoxia Induced Factors (HIFα) acquired from VHL loss can promote ccRCC tumorigenesis through regulating microRNAs (miRNA) expression. Here, we performed a miRNA profiling and used high throughput analysis to identify a panel of VHL dependent miRNAs in ccRCC. Validation of these miRNAs uncovered overexpression of miR-2355-5p in ccRCC cell models, and primary tumors. Moreover, we showed a significant increase of circulating miR-2355-5p in plasma from patients with ccRCC. Mechanistically, miR-2355-5p overexpression was confirmed to be HIF-2α-dependent. Indeed, targeting miR-2355-5p with the CRISPR/cas9 system did not only negatively disturbed ccRCC cell’s ability to stimulate angiogenesis, but also decreased cell proliferation and drastically reduced tumor growth in mice xenograft models. Finally, miR-2355-5p pulldown assay identified five tumor suppressor genes, ACO1, BTG2, CMTM4, SLIT2, and WDFY2, as potential targets. All five genes were significantly downregulated in ccRCC tumors and mice xenograft tumors. Results from this research demonstrate the oncogenic ability of miR-2355-5p and shed light on the possible route in which the miRNA controls angiogenesis and tumor growth in VHL-deficient ccRCC
2025-03-05 | GSE246950 | GEO
Project description:Post-transcriptional regulation of gene expression by miRNAs likely makes significant contributions to mRNA abundance at the embryo-maternal interface. In this study, we investigated how miR-26a-5p and miR-125b-5p contribute to molecular changes occurring in the uterine luminal epithelium, which serves as the first site of signal exchange between the mother and developing embryo. To measure de novo protein synthesis after miRNA delivery to primary uterine luminal epithelial cells, we employed pulsed stable isotope labeling by amino acids (pSILAC). We found that both miRNAs alter the proteome of luminal epithelial cells, impacting numerous cellular functions, immune responses, as well as intracellular and second messenger signaling pathways. Additionally, we identified several features of miRNA-mRNA interactions that may influence the targeting efficiency of miR-26a-5p and miR-125b-5p. Overall, our study suggests a complex interaction of miR-26a-5p and miR-125b-5p with their respective targets. However, both appear to cooperatively function in modulating the cellular environment of the luminal epithelium, facilitating the morphological and molecular changes that occur during the intensive communication between the embryo and uterus at pregnancy.
2025-05-07 | PXD056243 | Pride
Project description:Medulloblastoma (MB) is the most common malignant brain tumor in children. Despite recent improvements in overall survival, only a modest percentage of patients survive high-risk MB. The devastating side effects of radiation and chemotherapy substantially reduce qualify of life for surviving patients. We identified a novel tumor suppressor miRNA that sensitizes both ionizing radiation and vincristine responses in medulloblastoma. To understand the mechanism by which the tumor suppressor miR-584-5p may act as a tumor suppressor and therapy sensitizer, we performed microarray analysis in D425Med and D458Med medulloblastoma cells transfected with scrambled (miR-NC) or miR-584-5p mimic (miR-584-5p).
2018-12-26 | GSE105059 | GEO