Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA138087 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To metastasize, a tumor cell must acquire abilities such as the capacity to colonize new tissue and evade immune surveillance. Recent evidence suggests that microRNAs can promote the evolution of malignant behaviors by regulating multiple targets simultaneously. We performed a microRNA analysis of human melanoma, an aggressively invasive cancer, and found that miR-30b/30d upregulation correlates with stage, metastatic potential of primary tumors, shorter time to recurrence and reduced overall survival. Ectopic expression of miR-30b/30d promoted the metastatic behavior of melanoma cells by directly targeting the GalNAc transferase GALNT7, resulted in increased synthesis of the immunosuppressive cytokine IL-10, and reduced immune cell activation and recruitment. These data point to a key role of miR-30b/30d and GalNAc transferases in metastasis, by simultaneously promoting cellular invasion and immune suppression. MicroRNAs are emerging as key contributors to tumor metastasis because of their ability to regulate multiple targets, and thereby alter several functions, simultaneously. We found a miRNA cluster that promotes metastasis by concurrently enhancing invasive capabilities of melanoma cells and suppressing immune surveillance mechanisms, allowing the tumor cells to migrate and invade foreign tissue. Both these effects of miR-30b/30d are mediated by direct suppression of GalNAc transferases. Aberrant glycosylation has previously been connected to tumor progression, but the underlying molecular mechanisms and their impact on specific cellular pathways are poorly understood. Our work places the control of glycosylation as a novel molecular link between tumor cell migration and immune evasion, two processes that act synergistically during metastasis. 2 different melanoma cell line, 2 biological duplicates for each cell line Differentially expressed genes (mRNAs) in response to miRNA over-expression
2011-03-08 | E-GEOD-27718 | biostudies-arrayexpress
Project description:To metastasize, a tumor cell must acquire abilities such as the capacity to colonize new tissue and evade immune surveillance. Recent evidence suggests that microRNAs can promote the evolution of malignant behaviors by regulating multiple targets simultaneously. We performed a microRNA analysis of human melanoma, an aggressively invasive cancer, and found that miR-30b/30d upregulation correlates with stage, metastatic potential of primary tumors, shorter time to recurrence and reduced overall survival. Ectopic expression of miR-30b/30d promoted the metastatic behavior of melanoma cells by directly targeting the GalNAc transferase GALNT7, resulted in increased synthesis of the immunosuppressive cytokine IL-10, and reduced immune cell activation and recruitment. These data point to a key role of miR-30b/30d and GalNAc transferases in metastasis, by simultaneously promoting cellular invasion and immune suppression. MicroRNAs are emerging as key contributors to tumor metastasis because of their ability to regulate multiple targets, and thereby alter several functions, simultaneously. We found a miRNA cluster that promotes metastasis by concurrently enhancing invasive capabilities of melanoma cells and suppressing immune surveillance mechanisms, allowing the tumor cells to migrate and invade foreign tissue. Both these effects of miR-30b/30d are mediated by direct suppression of GalNAc transferases. Aberrant glycosylation has previously been connected to tumor progression, but the underlying molecular mechanisms and their impact on specific cellular pathways are poorly understood. Our work places the control of glycosylation as a novel molecular link between tumor cell migration and immune evasion, two processes that act synergistically during metastasis.
2011-03-08 | GSE27718 | GEO
Project description:We have employed microarray expression profiling as a discovery platform to identify microRNAs induced by radiation. Human A549 lung cancer cells were irradiated (2Gy/day for consistent 3days) and miRNA signature was identified that distinguished between control and radiation treated samples.Irradiated and un-irradiated A549 cells were harvested after 48 hr of treatment and microarray analysis was performed. Expression of five miRNAs (miR-30a, miR-30b, miR-30c, miR-30d, and miR-30d) from this signature was quantified in the same RNA samples by real-time PCR, confirming variability between control and radiation treated A549 cells.
2017-07-11 | GSE101085 | GEO
Project description:Milk composition is complex and includes numerous components essential for the offspring growth and development. Besides a high abundance of the miR-30b microRNA, milk produced by the transgenic mouse model of miR-30b-mammary deregulation displays significant changes in its fatty acid profils. Moreover, wild-type adopted pups fed with this milk present an early growth defect. Therefore, the consequences of miR-30b milk feeding on neonate gut development, a prime target of suckled milk, were investigated, along with further characterization of changes in milk composition. A broad characterization of the duodenum of wild-type pups fed with miR-30b milk was performed, using histological, transcriptomic, proteomic and intestinal permeability analyses. Milk of miR-30b foster dams was extensively analyzed using proteomic, metabolomic and lipidomic approaches and hormonal immunoassays. Pups fed with miR-30b milk showed a maturation of their gut tissue, presenting an earlier reduction in paracellular and transcellular permeability at postnatal day 5. MiR-30b milk displayed significant changes in its total lipid content, ceramides and sphingomyelin concentrations, an overabundance in nine proteins and an increase in insulin and leptin levels. These molecules were associated with neonatal gut integrity and maturation, notably by acting on tight junctions. Their significant changes in miR-30b milk could be clearly involved in the early intestinal closure phenotype of the pups, in connection with the observed early growth defect. Further investigations are now needed to determine their specific mode of action, with the aim to modulate infant diet in regard with a benefic effect on growth and health.
2023-10-09 | PXD037629 | Pride
Project description:Immunosuppression plays a crucial role in the development of cancer which remains a major cause of mortality in kidney transplant recipients. Cancer Exosomes (Exos) are extracellular vesicles described as modulators of tumor invasion and metastasis. This paper describes the effect of RAPA and CsA, two immunosuppressive drugs with different oncogenic proprieties, in Exos of colorectal cancer (CRC) cell lines. RAPA induces an increased Exos production and an overexpression of miR-6127, miR-6746-5p, and miR-6787-5p in Exos from a metastatic cell line. These miRNAs produce a significant down-regulation of epigenetic genes involved in cell cycle, chromatin and DNA regulation pre-metastatic niche. Our results describe a potential mechanism by RAPA in modulating pre-metastatic niche in post-transplant metastatic CRC through these exosomal miRNAs.
2019-08-20 | GSE123709 | GEO
Project description:Immunosuppression plays a crucial role in the development of cancer which remains a major cause of mortality in kidney transplant recipients. Cancer Exosomes (Exos) are extracellular vesicles described as modulators of tumor invasion and metastasis. This paper describes the effect of RAPA and CsA, two immunosuppressive drugs with different oncogenic proprieties, in Exos of colorectal cancer (CRC) cell lines. RAPA induces an increased Exos production and an overexpression of miR-6127, miR-6746-5p, and miR-6787-5p in Exos from a metastatic cell line. These miRNAs produce a significant down-regulation of epigenetic genes involved in cell cycle, chromatin and DNA regulation pre-metastatic niche. Our results describe a potential mechanism by RAPA in modulating pre-metastatic niche in post-transplant metastatic CRC through these exosomal miRNAs.
2019-08-20 | GSE123708 | GEO
Project description:Type 1 diabetes is an autoimmune disease characterized by the destruction of insulin-producing β-cells, leading to hyperglycemia. A temporary partial remission (PR) phase often follows diagnosis, marked by improved glycemic control and reduced autoimmunity. This study investigates the role of miR-30d-5p, a microRNA highly expressed during PR, on beta-cell recovery and regeneration. Remarkably, human pancreatic slices were successfully transfected with oligonucleotides (miR-30d-5p inhibitor or mimic), enabling exploration of post-transcriptional regulation in a human context. Bulk RNA sequencing on human pancreatic slices from 3 non-diabetic donors confirmed the regulation of gene networks linked to both β-cell function and regeneration. PCA revealed clustering by donor, indicating strong inter-donor variability; this was corrected using ComBat, allowing clearer separation of treatment groups. Differential expression analysis identified 273 DEGs for miR-30d-5p inhibition, 518 for overexpression, and 480 between the two treatments. Key gene changes reflected biological roles aligned with the miRNA’s proposed regulatory function: inhibition of miR-30d-5p upregulated genes linked to stress, immune activation, and metabolism (e.g., GLUT6, TGFB3, CYP4F8), while overexpression enhanced β-cell function and insulin secretion genes (e.g., HOOK1, ISL1, TTR, CACNB3). GO analysis showed that miR-30d-5p inhibition enriched pathways related to protein stress and impaired differentiation, whereas overexpression activated processes involved in ion homeostasis, morphogenesis, and β-cell maintenance. Transcription factor analysis highlighted FOXO3, NOTCH3, JUND, and NR1H2 as potential regulators. Overall, miR-30d-5p promotes β-cell survival, insulin synthesis, and immunoregulation.
2026-05-21 | GSE316801 | GEO
Project description:miRNAs are related with the initiation and development of prostate cancer. We discover the miR-195 and miR-30 can be as a biomarker of prognosis of prostate cancer in clinical patients. miRNA functions through affecting the mRNA degradation by binding the mRNA 3’UTR. So we test the change of transcriptional profile of miR-195 and miR-30d cell line respectively to further study the function of miR-195 and miR-30d. To study the function of miR-195 and miR-30d in prostate cancer, we setup the over-expression cell line of the miR-195 and miR-30d respectively in prostate cancer cell(LNCap and DU145), then study the change of transcriptional profile in cell line by microarray experiment (Affymetrix PrimeView human gene expression).
2016-08-23 | GSE85884 | GEO
Project description:Background & Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) is an independent risk factor for cardiovascular disease (CVD), although the mechanism underlying this association remains unclear. Extracellular vesicles (EVs) are biological nanoparticles that play critical roles in intercellular communication. We aimed to investigate the effects of hepatocyte-derived EVs on vascular endothelial cells in the context of MASLD. Methods: Primary hepatocytes were isolated and exposed under lipotoxic conditions. Human endothelial cells were treated with hepatocyte-derived EVs. Small RNA sequencing was performed to identify candidate microRNAs (miRs) responsible for hepatocyte-endothelial cell crosstalk. The in vivo effect of miR-30b-5p on atherosclerosis was tested in apolipoprotein E knock-out (ApoE-/-) mice. The level of miR-30b-5p in serum EVs was examined in human samples. Results: Treatment with EVs derived from palmitic acid-treated hepatocytes induced endothelial dysfunction in human endothelial cells, characterized by the upregulation of inflammatory cytokines, adhesion molecules, and oxidative stress markers. miR-30b-5p was identified as a candidate cargo, and its elevation was confirmed by qPCR in EVs from PA-treated hepatocytes and western diet-induced steatotic liver. ELOVL5, a key enzyme in fatty acid elongation, was identified as a direct target of miR-30b-5p. Overexpression of miR-30b-5p or knock-down of Elovl5 inhibited the elongation of polyunsaturated fatty acids (PUFAs), leading to endothelial inflammation, which was rescued by PUFA supplementation. Overexpression of miR-30b-5p accelerated atherogenesis in ApoE-/- mice, whereas downregulation of miR-30b-5p produced the opposite effect. miR-30b-5p levels in human serum-derived EVs were positively correlated with the fatty liver index. Conclusion: Hepatic steatosis accelerates vascular endothelial dysfunction and atherogenesis via EV-mediated activation of the miR-30b-5p/Elovl5 axis. Our findings suggest a novel mechanism explaining the independent relationship between MASLD and CVD.
2026-05-28 | GSE329384 | GEO
Project description:Objective: Trastuzumab has been used for the treatment of HER2-positive breast cancer (BC). However, a subset of BC patients exhibited resistance to trastuzumab therapy. Thus, clarifying the molecular mechanism of trastuzumab treatment will be beneficial to improve the treatment of HER2-positive BC patients. In this study, we identified trastuzumab-responsive microRNAs that are involved in the therapeutic effects of trastuzumab. Methods and results: RNA samples were obtained from HER2-positive (SKBR3 and BT474) and HER2-negetive (MCF7 and MDA-MB-231) cells with and without trastuzumab treatment for 6 days. Next, we conducted a microRNA profiling analysis using these samples to screen those microRNAs that were up- or downregulated only in HER2-positive cells. This analysis identified miR-26a and miR-30b as trastuzumab-inducible microRNAs. Transfecting miR-26a and miR-30b induced cell growth suppression in the BC cells by 40% and 32%, respectively. A cell cycle analysis showed that these microRNAs induced G1 arrest in HER2-positive BC cells as trastuzumab did. An Annexin-V assay revealed that miR-26a but not miR-30b induced apoptosis in HER2-positive BC cells. Using the prediction algorithms for microRNA targets, we identified cyclin E2 (CCNE2) as a target gene of miR-30b. A luciferase-based reporter assay demonstrated that miR-30b post-transcriptionally reduced 27% (p=0.005) of the gene expression by interacting with two binding sites in the 3’-UTR of CCNE2. Conclusion: In BC cells, trastuzumab modulated the expression of a subset of microRNAs, including miR-26a and miR-30b. The upregulation of miR-30b by trastuzumab may play a biological role in trastuzumab-induced cell growth inhibition by targeting CCNE2. We obtained microRNA expression profiles of breast cancer cell lines, MCF7, MDA-MB-231, SKBR3, and BT474, with or without trastuzumab (4microgram/mL) treatment.
2012-06-02 | E-GEOD-38415 | biostudies-arrayexpress