GEO 数据集
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- ISL1 and AQP5 complement each other to enhance gastric cancer cell stemness by regulating CD44 expressionGSE246329Homo sapiens12 个样本2026-10-31
Gastric cancer, a prevalent and life-threatening malignancy, is believed to involve cancer stem cells as a contributing factor to tumor progression. This study delves into the influence of ISL1 on the stem-like properties of human gastric cancer cells. In human gastric cancer samples, there is an observed elevation in ISL1 expression, which correlates with the expression of stem cell markers, notably LGR5. Functionally, ISL1 fosters the self-renewal, cell proliferation, migration, and the clonogenic potential of gastric cancer cells in vitro. Furthermore, it enhances the ability of these cells to form tumors and metastasize in vivo. Additionally, ISL1 collaborates with AQP5, collectively intensifying the tumorigenicity of gastric cancer cells. Mechanistically, transcriptomic analysis of cells overexpressing ISL1 unveils a notable activation of the FOXO pathway. This activation leads to increased nuclear expression of FOXO3, subsequently resulting in elevated expression of the stemness-associated gene CD44 in gastric cancer cells. These findings shed light on the role of ISL1 in promoting the stem-like characteristics of gastric cancer cells and emphasize the connection between ISL1 and AQP5 as a novel therapeutic target for individuals with gastric cancer.
- Identification of RNAs interacting with protein FovB in Escherichia coliGSE234102Escherichia coli CFT073; Escherichia coli J5312 个样本2026-10-31
The goal of this analysis was to identify the RNAs interacting with protein FovB which is encoded on IncI1 plasmid in two E. coli strains J53 and CFT073
- zebrafish retina m6A epitranscriptomeGSE186488Danio rerio4 个样本2026-10-31
m6A epitranscriptome of the retinas of adult zebrafish was sequenced using MeRIP-seq
- Microglia Secrete MiR-146a-5p-Containing Exosomes to Regulate Neurogenesis in DepressionGSE185777Rattus norvegicus6 个样本2026-10-31
Enhancing neurogenesis within the hippocampal dentate gyrus is critical for maintaining brain development and function in many neurological diseases. However, the neural mechanisms underlying neurogenesis in depression remain unclear. Here, we show that microglia transfer a microglia-enriched microRNA, miR-146a-5p, via secreting exosomes to inhibit neurogenesis in depression. Overexpression of miR-146a-5p in hippocampal dentate gyrus (DG) suppresses neurogenesis and spontaneous discharge of excitatory neurons by directly targeting Krüppel-like factor 4 (KLF4). Down-regulation of miR-146a-5p expression, ameliorates adult neurogenesis deficits in DG regions and depression-like behaviors in rats. Intriguingly, circular-RNA ANKS1B acts as a miRNA sequester for miR-146a-5p to mediate posttranscriptional regulation of KLF4 expression. Collectively, these results indicate that miR-146a-5p can function as a critical factor regulating neurogenesis under conditions of pathological processes resulting from depression and suggest that microglial exosomes generate new cross-talk channels between glial cells and neurons.
- mouse B16-F10 melanoma cells vs. Runx3 expressing B16-F10 cellsGSE161992Mus musculus1 个样本2026-10-31
Transcriptional profiling of the mock control mouse B16-F10 melanoma cells compares with that of the B16-F10 cells retrovirally expressing Runx3. Runx3 reduced the lung metastasis potential of the B16-F10 melanoma cells. This transcriptional profiling was used to uncover the differentially expressed genes that were regulated by Runx3.
- mouse B16-F0 melanoma cells vs. B16-F10 melanoma cellsGSE161991Mus musculus1 个样本2026-10-31
Transcriptional profiling of the mouse B16-F0 melanoma cells compares with that of mouse B16-F10 melanoma cells. B16-F10 melanoma cell line has very strong lung metastasis potential. B16-F10 melanoma cell line origninates from B16-F0, the later of which has very weak lung metastis potential. This transcriptional profiling was used to uncover the differentially expressed genes that may be associated with the acquirement of lung metastasis potential of B16-F10 cells.
- Genome-wide DNA methylation analysis in colorectal tumor and normal tissuesGSE159670Homo sapiens24 个样本2026-10-31
The current risk stratification system defined by clinicopathological features do not accurately identify the risk of disease recurrence in patients with stage I-II colorectal cancer (CRC). We aimed to investigate whether the CpG sites from newly established genome-wide methylation profiles could serve as biomarkers to improve prognosis prediction.
- eCLIP-seq profiling of Flag-OTUD6B-associated RNA in HEK293T cellsGSE352643Homo sapiens4 个样本2026-10-30
RNA associated with Flag-OTUD6B was profiled by enhanced crosslinking and immunoprecipitation sequencing (eCLIP-seq) in human HEK293T cells. Two independent biological replicates were represented by two FLAG immunoprecipitation libraries and two corresponding size-matched input (SMInput) control libraries. This experiment and the OTUD6B-knockdown Ribo-seq experiment in MDA-MB-231 cells belong to the same research study.
- Ribosome profiling of OTUD6B knockdown and scramble-control MDA-MB-231 cellsGSE352635Homo sapiens4 个样本2026-10-30
Ribosome profiling was performed in human MDA-MB-231 cells with shOTUD6B-41 or a scramble-control shRNA. Two independent biological replicates were included per group, yielding four paired-end sequencing libraries. Gene-level read counts and FPKM expression values were generated. This experiment and the Flag-OTUD6B eCLIP-seq experiment in HEK293T cells belong to the same research study.
扰动筛选 - The metabolic reprogramming of T cells controls airway remodeling in severe asthmaGSE352552Mus musculus10 个样本2026-10-30
Background: Mixed granulocytic asthma (MGA) is a severe Th2-low endotype, characterized by high Th17/neutrophilic burden and exacerbated airway remodeling. Both features confer resistance to inhaled corticosteroids and typical asthma treatments. Objective: We aimed to address gaps in knowledge, including how Th17 cells induce pathological tissue remodeling and how Th17 differentiation occurs in response to allergens. Methods: We generated a Th2-low murine model of asthma on the Il4rα-/- background that mimics the decrease in type 2 response seen in corticosteroid-resistant patients. We monitored major features of human disease including heightened airway reactivity to methacholine, Th17/neutrophilic inflammation, airway remodeling, and resistance to corticosteroid treatment. Comparative transfer of Th2 versus Th17 cells were analyzed. We further investigated how the mitochondrial oxidative phosphorylation (OXPHOS) pathway modulates pathogenic Th17 cell reprogramming by in vitro T cell cultures and in vivo therapeutic blockades. Results: LIGHT (aka TNFSF14) and the OXPHOS pathway are enriched in human MGA and likewise upregulated in this mouse model. We show OXPHOS promotes the metabolic reprograming of Th17 cells, to sustain their survival despite steroid treatment and produce LIGHT that controls airway remodeling. Mechanistically, OXPHOS regulates RORγt expression and the subsequent transcriptional network to program differentiation of Th17 cells, whereas LIGHT drives airway remodeling by activating the MMP9-dependent TGFβ pathway. Additionally, OXPHOS+Th17 cells promote the expression of osteopontin necessary for fibroblast activation. LIGHT antagonistic blockade reduces airway remodeling, whereas OXPHOS inhibition kills Th17 cells and subsequent neutrophilia. Importantly, the dual blockade of LIGHT and OXPHOS reverses all features of MGA back to baseline and reciprocally increases the numbers of Treg cells. Conclusions: The dual blockade of LIGHT and OXPHOS constitutes a promising target for clinical interventions in human MGA, possibly extending to other Th17-driven fibrotic diseases.
- Cilengitide limits the progression of both syndromic and sporadic thoracic aortic aneurysms by targeting alpha V integrinsGSE352523Homo sapiens11 个样本2026-10-30
Spatial transcriptomics was used to characterize gene expression patterns in human ascending aortic tissue from healthy controls, patients with Marfan syndrome (MFS), and patients with sporadic thoracic aortic aneurysm (sTAA). Carnoy-fixed, paraffin-embedded ascending aortic tissue sections were profiled using the 10x Genomics Visium platform. Spatially resolved gene expression profiles were analyzed to investigate transcriptional heterogeneity, pathway-associated signatures, and inferred cellular composition across disease groups.
单细胞空间转录组 - Alcohol-induced suppression of miR-1948-3p promotes an adaptive HIF-1α response to limit hepatic steatosisGSE352328Mus musculus8 个样本2026-10-30
To investigate the role of HIF-1α in alcohol-associated liver disease, we performed transcriptomic profiling on liver tissues from chronic alcohol-fed mice (AF) and mice with hepatocyte-specific Hif-1α knockdown (AF+Hif-1α KD). RNA-seq analysis revealed that Hif-1α deficiency markedly altered the hepatic transcriptional landscape and identified the disruption of the PPAR signaling pathway. Overall, this dataset provides insights into the molecular mechanisms by which HIF-1α limits hepatic steatosis during alcohol exposure.
- Effects of orexin-A on human dermal papilla cellsGSE352146Homo sapiens6 个样本2026-10-30
We examined effects of orexin-A on human dermal papilla cells.
- Adaptive transcriptional responses to KRAS(G12C) inhibition in cancer cellsGSE352065Homo sapiens60 个样本2026-10-30
KRAS(G12C) inhibitors have demonstrated promising antitumor activity, but adaptive resistance remains a major therapeutic challenge. To characterize transcriptional adaptations to KRAS(G12C) inhibition, we performed bulk RNA sequencing of four human KRAS(G12C)-mutant cancer cell lines (H358, Calu-1, H23, and H1792) following treatment with RMC-6291. Transcriptomic analyses were conducted to identify treatment-associated gene expression changes and biological pathways, with particular emphasis on metabolic reprogramming and glutathione-associated responses. This dataset provides insights into the transcriptional responses of cancer cells to KRAS(G12C)-targeted therapy.
- StrataChip: a microphysiological system to capture dynamic keratinocyte fate and mechanical transitions during human epidermal morphogenesisGSE351999Homo sapiens1 个样本2026-10-30
Epidermal development and homeostasis require precise coordination between keratinocyte differentiation and mechanics. Still, the mechanisms integrating these processes remain poorly understood in part due to limitations of existing experimental systems. Here, we introduce StrataChip, a tractable microphysiological system that enables dynamic, multimodal interrogation of human epidermal morphogenesis. The platform integrates a media perfused dermal tissue with human epidermal keratinocytes within a microfluidic device and supports rapid epidermal stratification following establishment of an air-liquid interface. High-resolution confocal imaging and single-cell RNA-sequencing demonstrate that the StrataChip recapitulates key architectural and molecular features of human epidermis, including distinct basal, spinous, and granular layers defined by canonical differentiation markers and adhesion molecule organization. Single-cell profiling reveals transcriptionally distinct basal and spinous subpopulations, including transitional states associated with suprabasal commitment. Live 3D imaging in situ captures keratinocyte morphodynamics including basal cell delamination and asymmetric division in early stages of epidermal stratification. Altogether, StrataChip provides a robust platform that is capable of dynamic and mechanistic interrogation of how gene regulation and cell mechanical changes are coupled during epidermal morphogenesis.
单细胞 - T cell responses distinguish the subset of oral dysplasia that progressed to cancerGSE351967Homo sapiens16 个样本2026-10-30
The factors that determine which oral premalignant lesions progress to cancer while others do not remain unclear. Immune responses to early lesions result in cancer immunoediting, so variability in their nature and strength may influence risk of cancer progression. Here, we show that T cell-mediated immune responses arise in oral premalignant dysplasia years before invasive cancer develops and distinguish lesions that progress from those that do not. Progressing lesions were characterized by robust infiltration of CXCL13+ CD8 T cells in proximity to dysplastic epithelial cells and macrophages expressing interferon-stimulated genes (ISGs), including the T cell-recruiting chemokines CXCL9, CXCL10, and CXCL11. Infiltrating CXCL13+ CD8 T cells were clonally expanded and persisted through malignant transformation. Over time, their frequency and transcriptional profile remained stable, while myeloid cells accumulated and basal epithelial cells upregulated an extracellular matrix-associated transcriptional program partly induced by IFNγ. The transition to invasive cancer was subsequently marked by tissue remodeling accompanied by a shift of the CXCL13+ CD8 T cells from the epithelium to the underlying stroma. Our results provide evidence that IFNγ-driven immune signatures are detectable early and distinguish progressing oral lesions.
- Heterogeneity and interaction of microglia and macrophages after retinal detachmentGSE351957Mus musculus5 个样本2026-10-30
This study aims to systematically investigate the evolutionary processes of microglia and macrophages during the onset and progression of retinal detachment (RD).
- Elucidation of the anti-neuroinflammatory effect of M4FQA in HMC3 cellsGSE351949Homo sapiens12 个样本2026-10-30
These study demonstrate that M4FQA attenuates LPS-induced microglial inflammation through coordinated modulation of NF-κB-associated transcriptional networks and suggest that interaction with the TLR4/MD-2 system may contribute to its anti-inflammatory activity. M4FQA therefore emerges as a promising CQA-derived therapeutic candidate for further investigation in the treatment of neuroinflammatory disorders. Pretreatment of 1µM M4FQA significantly attenuated LPS-induced expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. Transcriptomic analysis demonstrated that pretreatment of M4FQA markedly modulated the LPS-induced transcriptional profile, with prominent regulation of genes associated with NF-κB-related inflammatory signaling, cytokine and chemokine responses, cellular homeostasis, and MAPK-associated pathways. M4FQA also reduced the expression of NF-κB-associated inflammatory chemokines, including CCL2, CXCL8, and CXCL6, while functional analyses identified additional modulation of genes associated with synaptic organization and signaling. Molecular docking predicted favourable interaction of M4FQA with the TLR4/MD-2 complex, and SPR analysis further supported interaction with the TLR4 target.
- Single-cell RNA sequencing of pooled orthotopic pancreatic tumors derived from PKM2-WT and PKM2-K89R cellsGSE351631Mus musculus2 个样本2026-10-30
We performed single-cell RNA sequencing of orthotopic pancreatic tumors established in NCG mice using pancreatic cancer cells expressing wild-type PKM2 (PKM2-WT) or the lactylation-deficient PKM2 K89R mutant (PKM2-K89R). For each group, tumor tissues from five mice were pooled before single-cell library preparation, resulting in one library per group. The dataset was used to characterize the tumor microenvironment and compare cell-type composition and cellular transcriptional states between the PKM2-WT and PKM2-K89R groups, with particular focus on fibroblast and cancer-associated fibroblast (CAF) subpopulations.
单细胞 - Transcriptomic profiling of human nucleus pulposus cells following Mulberrin treatmentGSE351312Homo sapiens6 个样本2026-10-30
This study profiled the transcriptomes of human nucleus pulposus cells with or without Mulberrin treatment to identify gene expression changes associated with Mulberrin exposure. genes and exploring molecular pathways potentially involved in the cellular responses to Mulberrin treatment.
- White Collar proteins AoLreA and AoLreB coordinate light-responsive conidiation and pathogenicity in Arthrobotrys oligosporaGSE350352Orbilia oligospora12 个样本2026-10-30
Light is a major environmental cue for filamentous fungi, yet the contribution of canonical White Collar proteins to the specialized development of nematode-trapping fungi remains poorly understood. Here, we characterized the White Collar homologs AoLreA and AoLreB in Arthrobotrys oligospora using gene deletion, light-dependent phenotyping, microscopy, protein-interaction assays, and transcriptomics. Both deletion mutants produced few conidia in darkness but abundant conidia under white light, accompanied by altered conidial morphology and spore-related gene expression. Furthermore, AoLreA interacted with AoLreB, whereas AoLreB also interacted with the velvet regulator AoVeA, linking the White Collar module to a broader developmental network. Beyond sporulation, ΔAolreA formed more traps and displayed enhanced pathogenicity, while ΔAolreB had comparatively limited effects on nematode predation. Cellular analyses further revealed altered vacuolar organization in ΔAolreA and an accumulation of autophagy-associated structures in ΔAolreB. Transcriptomic comparisons of WT and ΔAolreA strains under light and dark conditions revealed extensive transcriptional changes associated with carbohydrate and polysaccharide metabolism, cell-wall organization, hydrolase and oxidoreductase functions, and secondary metabolism. Together, these results identify AoLreA and AoLreB as functionally distinct light-responsive developmental regulators in A. oligospora.
- Empowering multiplexed ultra-throughput ribosome profiling with RiboWichGSE350000Homo sapiens; Mus musculus33 个样本2026-10-30
Ribosome profiling has improved the understanding of mRNA translation, enabling single-nucleotide resolution mapping of ribosome positioning along transcripts. However, most ribosome profiling methods remain labor-intensive, inefficient, and low-throughput, limiting scalability and broader adoption. Here, we develop RiboWich (Ribosome sandWich), a streamlined approach that directly ligates adaptors to ribosome-embedded RNA fragments, bypassing the need for ribosome purification and footprint size-selection, tackling two major bottlenecks. Through a dual-step multiplexing strategy, RiboWich supports automated 384-well profiling while retaining sensitivity and capturing condition-specific differences in translation. By enabling scalable, low-input, and automated translatome profiling, RiboWich provides a versatile and accessible platform for ultra-throughput and future single-cell ribosome profiling applications.
单细胞 - Inactivation of Irs1 in pericentral hepatocytes promotes lipid oxidationGSE349448Mus musculus4 个样本2026-10-30
Hepatic metabolic zonation enables periportal (PP) and pericentral (PC) hepatocytes to perform distinct functions in glucose and lipid metabolism. Insulin signaling is also spatially organized across the liver lobule, but the transcriptional role of insulin signaling in PC hepatocytes remains incompletely understood. To define the gene-expression programs regulated by insulin signaling in PC hepatocytes, we generated mice with inducible PC-specific deletion of insulin receptor substrate 1 (Irs1) using Cyp1a2CreER (Irs1-Cyp1a2 mice). RNA sequencing was performed to compare liver gene-expression profiles between Irs1-Cyp1a2 mice and littermate controls. This dataset provides a transcriptomic resource for identifying pathways regulated by PC IRS1 signaling and for understanding how spatial insulin signaling contributes to hepatic glucose and lipid metabolism.
空间转录组 - HFpEF HMDP: ventricular RNA-seq in an expanded BXD strain panelGSE348752Mus musculus194 个样本2026-10-30
Systems genetics strategy across multiple Hybrid Mouse Diversity Panel (HMDP) cohorts. RNA sequencing of ventricles from HFpEF mice was performed primarily in an expanded panel of BXD strains, together with a small number of classic inbred strains. This submission represents the expanded BXD component of the HFpEF HMDP project.
- GPS2 attenuates cigarette smoke-induced airway epithelial injury by attenuating mitochondrial oxidative stressGSE347944Homo sapiens6 个样本2026-10-30
Cigarette smoke (CS) exposure contributes to airway epithelial injury and mitochondrial dysfunction in chronic obstructive pulmonary disease (COPD). G protein pathway suppressor 2 (GPS2) is involved in mitochondrial-nuclear communication, but its role in cigarette smoke-induced airway epithelial injury remains unclear. In this study, transcriptome sequencing was performed to investigate the molecular changes associated with GPS2 deficiency in airway epithelial cells and to explore the potential mechanisms linking GPS2 to mitochondrial dysfunction and epithelial injury. Combined with public transcriptomic data and experimental validation, our results suggest that reduced GPS2 expression is associated with alterations in energy metabolism, mitochondrial function, and redox homeostasis. These data provide a transcriptomic resource for further investigating the role of GPS2 in cigarette smoke-induced airway epithelial dysfunction.
- Early Pitx2 modulation of Fgf10 directs asymmetric lung morphologyGSE347452Mus musculus8 个样本2026-10-30
Both the molecular cascade establishing Left-Right asymmetric anatomy, including the transcription factor Pitx2, and the signaling pathways controlling branching morphogenesis of the lung (a Left-Right asymmetric process) have been intensively studied. However, the two have never been linked. We identify Fgf10 as a Pitx2-sensitive signal in the mesenchyme of the developing mouse lung. Pitx2 suppresses Fgf10 expression, making the right lung, which lacks Pitx2 expression, grow faster than the left during the budding stage. Modulating Fgf10 dosage in the left mesenchyme is sufficient to shift levels of epithelial proliferation and thereby alter lung budding asymmetry. Pitx2 activity during the earliest lung bud stages is sufficient to establish differences in the primary airway branches, leading to subsequent asymmetric branching patterns that eventually manifest as the left-right differences in lung morphology. Thus, Pitx2 converts left-right mesenchymal identity into organ asymmetry by quantitatively tuning Fgf10-dependent epithelial growth during early lung organogenesis.
- RNA-sequencing of brain endothelial cells from Slc1a1 endothelial cell conditional knockout mice and controlsGSE346752Mus musculus8 个样本2026-10-30
The goal of this study was to understand the transcriptional response of brain endothelial cells to a loss of brain endothelial Slc1a1 expression. Sample GSM10039984 (ECs, control, 3) and GSM10039987 (ECs, mutant, 4) were excluded from all published analyses because of separation from its group on principal component analysis. Final analyses used n = 3 per group. The excluded sample is included in this deposition for completeness.
- Ribosome profiling of clear cell renal cell carcinoma tumor and adjacent normal kidney tissue samplesGSE346551Homo sapiens10 个样本2026-10-30
Despite growing recognition that non-canonical open reading frame (ncORF)-encoded micropeptides constitute a hidden layebiological functions, and therapeutic relevance in renal cell carcinoma (RCC) remain entirely undefined. Through integrative transcriptomic, translatomic, and proteomic profiling of clinical RCC specimens, we systematically mapped the dysregulated ncORF-encoded micropeptidome and identified long non-coding RNAs (lncRNAs) as a predominant source of tumor-associated cryptic peptides. These findings illuminate a therapeutically actionable micropeptide-mediated regulatory network in RCC and establish ncORF-encoded tumor suppressors as a druggable class of biologics for precision oncology.r of functional regulators in cancer, their translational landscape,
- RNA-seq of clear cell renal cell carcinoma tumor and adjacent normal kidney tissue samples.GSE346548Homo sapiens10 个样本2026-10-30
Renal cell carcinoma (RCC) is among the most common urological malignancies, yet the transcriptomic landscape underlying its pathogenesis remains incompletely characterized, particularly for non-coding regions that may harbor functional non-canonical open reading frames (ncORFs). Here we performed whole-transcriptome RNA-seq on 5 clear cell RCC tumor tissues and 5 adjacent normal kidney tissues to systematically profile mRNA, lncRNA, and circRNA expression. This dataset serves as the transcriptomic layer of an integrative multi-omics study aimed at identifying dysregulated ncORF-encoded micropeptides in RCC, with lncRNAs representing a predominant source of tumor-associated cryptic peptides. The data provide a reference for translational activity assessment when combined with matchedribosome profiling and immunopeptidomics datasets.
多组学 - Late-gestation heat stress induces gene expression and persistent DNA methylation changes in the mammary gland parenchyma at birth and weaningGSE346246Bos taurus64 个样本2026-10-30
This SuperSeries is composed of the SubSeries listed below.
SuperSeries