GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• Geometric inference of cross-species transcriptome correspondence
  GSE307647Gorilla gorilla; Pan troglodytes; Homo sapiens; Macaca fascicularis; Pongo abelii; Mus musculus28 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Geometric inference of cross-species transcriptome correspondence [RNA-Seq]
  GSE307646Macaca fascicularis; Homo sapiens22 个样本2026-10-31

  Sequence homology underpins cross-species analysis but cannot identify evolutionarily distinct genes that play analogous regulatory roles. Furthermore, ethical restrictions on human experiments necessitate analytical frameworks that translate insights from other animals to humans. To address these challenges, we develop Species-OT, a cross-species transcriptome analysis framework based on Gromov-Wasserstein optimal transport, which quantitatively compares the geometry of transcriptome distributions. Given a pair of bulk or single-cell RNA-sequencing datasets, Species-OT returns a gene-to-gene correspondence capturing probabilistic alignments of regulatory roles, and a transcriptomic distance quantifying overall divergence. Applied pair wise, Species-OT yields a transcriptomic discrepancy array and a hierarchical clustering tree analogous to a phylogenetic tree. We validate Species-OT using bulk RNA-seq data from human, mouse, and macaque germ cell specification as well as scRNA-seq data from pluripotent stem cells of six mammalian species. Species-OT identifies evolutionarily related and distinct gene correspondences including biologically unexplored candidates, while transcriptomic discrepancies recapitulate expected species relationships.

  单细胞
• Geometric inference of cross-species transcriptome correspondence [scRNA-Seq]
  GSE307645Macaca fascicularis; Pan troglodytes; Gorilla gorilla; Pongo abelii; Homo sapiens; Mus musculus6 个样本2026-10-31

  Sequence homology underpins cross-species analysis but cannot identify evolutionarily distinct genes that play analogous regulatory roles. Furthermore, ethical restrictions on human experiments necessitate analytical frameworks that translate insights from other animals to humans. To address these challenges, we develop Species-OT, a cross-species transcriptome analysis framework based on Gromov-Wasserstein optimal transport, which quantitatively compares the geometry of transcriptome distributions. Given a pair of bulk or single-cell RNA-sequencing datasets, Species-OT returns a gene-to-gene correspondence capturing probabilistic alignments of regulatory roles, and a transcriptomic distance quantifying overall divergence. Applied pair wise, Species-OT yields a transcriptomic discrepancy array and a hierarchical clustering tree analogous to a phylogenetic tree. We validate Species-OT using bulk RNA-seq data from human, mouse, and macaque germ cell specification as well as scRNA-seq data from pluripotent stem cells of six mammalian species. Species-OT identifies evolutionarily related and distinct gene correspondences including biologically unexplored candidates, while transcriptomic discrepancies recapitulate expected species relationships.

  单细胞
• Transcriptomic changes from resulting from treatment of SVG-A with drugs of abuse
  GSE306251Homo sapiens21 个样本2026-10-31

  SVG-A cells were treated with drugs of abuse (ethanol, cocaine, morphine, THC, and psilocin) prior to RNA sequencing. A bioinformatics pipeline of Trim Galore, Kallisto, DESeq2 and Qiagen Ingenuity Pathway Analysis was used for pathway analysis.
• Disruption of nucleolar integrity triggers cellular quiescence through organelle rewiring and secretion
  GSE305361Homo sapiens27 个样本2026-10-31

  Intrinsic cellular stress responses are often mis regulated in complex human diseases such as cancer and neurodegeneration. To investigate how cellular homeostasis is balanced upon loss of key membraneless organelle – Nucleolus, we performed unbiased systems approach including cellular and temporal characterization of activated cellular stress signaling, associated sub-cellular changes and changes in cellular states and behavior. We report that transient loss of nucleolar architecture and defective ribosome biogenesis is well tolerated by cells as they undergo prolonged cell cycle arrest and rely on buffering capacity of cytoplasmic translation machinery. Cells immediately mount a comprehensive stress response predominantly mediated by TP53 and its downstream effector proteins. This mounted stress response is distinct from other acute stresses altering nucleolar morphology or function such as Pol I inhibition by ActD, heat shock or chemicals like Arsenate and CPT. Cells show a robust transcriptional reprogramming showing upregulation of structural and signaling genes of organelles such as Golgi apparatus and Endo-lysosomal vesicles. This leads to translation and microscopically evident tubular-vesicular expansion of Golgi and increase in number and size of endo-lysosomes. Cells become secretory, pro-metastatic and alter their cell-to-cell communication behavior. Taken together, these stress response pathways show an adaptive quiescent program and acquired partial EMT, allowing cells to resist loss of ribosome biogenesis, nucleolar architecture and ensure survival and restore homeostasis upon recovery. Correlatively, similar stress adaptions are seen to be contributing to progression of different cancer types especially in breast cancer and AML originating in the later stages of ribosomopathies.
• Determination of transcriptomic changes associated with salt stress in ethanol-treated control plants and TRB3-SRDX mutants.
  GSE302039Arabidopsis thaliana32 个样本2026-10-31

  Soil salinization severely threatens crop productivity. We previously revealed that ethanol treatment enhances abiotic stress tolerance, including salt stress, in plants. Ethanol up-regulated the transcription and activity of ascorbate peroxidase (APX1/2), key ROS detoxifing enzymes, thereby reducing ROS accumulation and improving salt stress tolerance. However, the transcriptional regulation underlying ethanol-mediated stress tolerance remains unclear. In this study, we identified Telomere repeat binding (TRB) proteins as transcription factors involved in ethanol-mediated salt stress tolerance. Transcriptome analysis revealed that copper/zinc superoxide dismutase (CSD) genes were down-regulated in TRB3-SRDX mutant. We further demonstrated that SOD activity was reduced in trb1/2/3 mutantm and csd mutant showed salt stress sensitivity even presence with ethanol, indicating that CSD are essential for ethanol-mediated salt stress tolerance. ChIP assays confirmed that TRB3 directly binds to CSD genes. Furthermore, ethanol treatment promoted H4K5 acetylation at CSD loci. These findings suggests that ethanol metabolism contributes to histone acetylation, and TRB3 facilitates its deposition at CSD loci, leading to enhanced CSD activation and improved salt stress tolerance.
• scRNA-seq of skin and PBMC samples of systemic sclerosis patients and healthy controls
  GSE299141Homo sapiens20 个样本2026-10-31

  Skin and blood samples from systemic sclerosis (SSc) patients and healthy donors were analyzed using single-cell transcriptomics (scRNA-seq). CCL19+ fibroblast was upregulated in the dermis of patients with SSc, and exhibited high expression of immuno-regulatory genes, including CCL19. CCL19 expression correlated with the severity of dermal fibrosis in SSc. The most significant ligand-receptor interaction from CCL19+ fibroblast to T cells in SSc skin was CCL19-CCR7. Furthermore, CCR7+ T cells in the fibrotic skin, particularly CCR7+CD8+ T cells, displayed enhanced stemness and cytotoxicity, actively interacting with extracellular matrix (ECM)-producing fibroblasts in SSc.

  单细胞
• Transcriptomic responses of zebrafish following dietary exposure to the short chain PFAS perfluorohexanoic acid (PFHxA)
  GSE291637Danio rerio19 个样本2026-10-31

  Per- and polyfluoroalkyl substances (PFAS) have garnered tremendous concern due to the widespread contamination and environmental persistence as PFAS and their heavy use in commercial products. While the properties of PFAS are useful for various consumer goods, the same properties result in high persistence of PFAS in the environment as well as an increased risk of exposure and deleterious effects for humans and ecosystems. To address data gaps for less studied PFAS, the use of molecular tools is essential to identify novel toxicity pathways that help to reduce additional animal testing for this large chemical class. In our current study, we exposed a model species (zebrafish) to a short chain PFAS, perfluorohexanoic acid (PFHxA), via the diet, which is an understudied exposure route in fish. Fish were exposed over 28 days to a measured low dietary dose (57.6 ng/g) as well as a higher dose (60.7 ng/g). At the end of the exposure, liver tissues were processed for mRNA and libraries were prepared for RNA-seq analysis. In addition to the transcriptome, qPCR will be performed to further assess changes in gene expression due to PFHxA dietary exposure. This study will be the first to examine sub-chronic dietary exposures to PFHxA and the resulting impacts on the transcriptome.
• RNA Immunoprecipitation Sequencing (RIP-seq) of RNAs associated in vivo with the FopA protein performed in Escherichia coli J53 or CFT073
  GSE290169Escherichia coli J53; Escherichia coli CFT07336 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Identification of RNAs interacting with protein FopA in Escherichia coli [RIP-Seq]
  GSE290168Escherichia coli CFT073; Escherichia coli J5324 个样本2026-10-31

  The goal of this analysis was to identify the RNAs interacting with protein FopA which is encoded on IncI1 plasmid in two E. coli strains J53 and CFT073
• Social Stress Differentially Affects the Behavior and the Transcriptome of the adBNST between Male and Female Mice.
  GSE287634Mus musculus20 个样本2026-10-31

  Stress can be broken down into systemic and processive stressors with processive stressors requiring higher limbic processing. These are also often called social stressors as they require an understanding of social dynamics as opposed to physical based stressors. This differing of processing necessitates we study both phenomena. Additionally, sex is an important aspect of stress research as men and women show differing responses to stress and mood disorder development. To study this, we used a chronic social instability stress (CSIS) paradigm to stress male and female mice. This paradigm is approximately 7-weeks long and involves changing the cage mates of a mouse every 3 days so stable social dynamics cannot form. Afterwards, one cohort was used for avoidance behavior testing using the open field test, the elevated plus maze, the light/dark box emergence test, and the novelty suppressed feeding test. A second cohort was used for bulk RNA-Sequencing of the anterodorsal bed nucleus of the stria terminalis which is a limbic structure known to be related to chronic stress signaling. In the behavior assays, CSIS caused the females to be less avoidant, while the males became more avoidant. Additionally, we found that a low estrogen state in the females caused them to be less avoidant than in a high estrogen state. In the transcriptome, we found major differences between the males and females with the males expressing more genes related to transcription whereas the females expressed more genes related to synaptic transmission. We also found that the transcriptome in the males is more sensitive to the stress than the females. In summary, we have found how social stress is differentially regulated between males and females and how this may be related to the development of stress-related behavioral changes.
• Comparative analysis of RLR-specific RNA ligands during influenza virus infection
  GSE287560Homo sapiens; Influenza A virus (A/Guangdong-Maonan/51/2009(H1N1))48 个样本2026-10-31

  RIG-I-like receptors (RLRs) play a critical role in detecting RNA virus infections and initiating antiviral immune responses. This study examined the roles of three RLRs—RIG-I, MDA5, and LGP2—in recognizing wild-type (WT) influenza virus infections and characterized their RNA ligands at both the nucleotide sequence and post-transcriptional modification levels. Our findings indicate that RIG-I and MDA5 are essential for sensing influenza A (IAV) and influenza B (IBV) viruses. RNA ligands isolated from RIG-I and LGP2 demonstrated immunostimulatory activity in type I interferon (IFN) reporter assays. Specifically, RIG-I bound to RNA sequences within the negative-sense NS and M segments of the influenza virus, while LGP2 interacted exclusively with the negative-sense 5′ and 3′ ends of the M segment. Notably, the viral segments were more potent in activating type I IFN signaling than their positive-sense counterparts, which aligns with the IC50 values of the NS and M segments binding to RIG-I. Additionally, in IAV-infected cells, RIG-I selectively recognized RNA polymerase III transcripts, which exhibited decreased 5-methylcytosine (m5C) modification levels upon infection. These results highlight the contributions of both viral and host RLR ligands to anti-influenza virus immunity, emphasizing their specific sequences and the NSUN2-mediated post-transcriptional modification profile. Overall, this study provides a comprehensive view of RLR-mediated sensing mechanisms that regulate antiviral responses to influenza virus infections.
• Nephrin-associated phospho-protein network necessary for filtration at the slit-diaphragm and podocyte adhesion.
  GSE284774Mus musculus25 个样本2026-10-31

  Minimal Change Disease (MCD) is characterized by nephrotic syndrome. In a subgroup of patients, pathogenic antibodies against the slit-diaphragm (SD) protein Nephrin encoded by the gene NPSH1 were identified in blood and biopsy samples. Nephrin is essential for the SD as specific NPHS1 variants result in congenital nephrotic syndrome. Intact Nephrin is a structural component of the SD, but also transmits signals to the actin cytoskeleton of podocyte foot processes (FP) thereby presumably stabilizing podocyte FP morphology. Thus, analyzing the Nephrin signalosome is attractive to identify potential targets for therapeutic intervention in MCD. We employed a model of MCD with antibody-mediated clustering of Nephrin leading to tyrosine phosphorylation-dependent signal transduction in podocyte culture. Phospho-proteome analysis after antibody-mediated Nephrin clustering revealed approx. 180 differentially phosphorylated peptides. Gene set analysis showed that among others the biological process ‘cell matrix adhesion’ was enriched. We verified that two thirds of the identified proteins were necessary for filtration in vivo employing a knockdown approach with consecutive analysis by an in-vivo filtration assay in Drosophila melanogaster nephrocytes. One of the phosphorylated proteins following Nephrin activation in the phospho-proteome analysis was the activating factor of the small GTPase Rap1 – Rapgef1. The significance of this Nephrin effector Rapgef1 for SD and focal adhesion integrity was exemplary studied generating a Rapgef1 knockout (Rapgef1KO) in the metanephric mesenchyme of mice. We confirmed that an early Rapgef1 knockout in podocytes - like transgenic Nephrin mice deficient in tyrosine-dependent signaling – resulted in nephrotic syndrome and an MCD/focal segmental glomerulosclerosis (FSGS) phenotype. RNA sequencing of Rapgef1 knockout mice glomeruli revealed significant regulation of genes involved in cell signaling, cell adhesion, and extracellular matrix organization. Changes in glomerular basement membrane (GBM), focal adhesion (FA) composition, and significant podocyte loss were confirmed by immunofluorescence analysis in Rapgef1 knockout mice glomeruli. Altogether, we identified a Nephrin-associated phospho-protein network necessary for filtration at the slit-diaphragm and podocyte adhesion.
• SUMOylation of SND1 promotes degradation of novel tumor suppressive miRNAs in cancer cells
  GSE281560Homo sapiens16 个样本2026-10-31

  Endonuclease Staphylococcal nuclease domain-containing protein 1 (SND1) was reported mediate miRNA decay of both protein-free and AGO2-loaded miRNAs. We recently found that SUMOylation of SND1 is involved in the regulation of the mature miRNA decay. The in vivo and in vitro SUMOylation assay have proven that SND1 can be modified by SUMO1 at the major site K513, and this modification can be enhanced upon the sodium arsenite and heat shock. Mutation K513R of SND1 inhibits cell proliferation and colony formation of H1299 cells under both normal and sodium arsenite stimulated conditions. Our data demonstrate that miRNA metabolism is connected to cellular stress response and tumorigenesis through the reversible SUMOylation of SND1. The stress-induced SND1 SUMOylation can degrade miRNA to regulate mRNA homeostasis, which may be a key node in the stress survival strategy.
• Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells
  GSE280503Homo sapiens6 个样本2026-10-31

  In this study, transient transcriptome sequencing (TT-seq) was performed to dectect the impact of the overexpression of CTCF-s on nascent RNA and antisense RNA.
• BL-Hi-C, Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells
  GSE280419Homo sapiens8 个样本2026-10-31

  In this study, we performed BL-Hi-C to investigate the influence of the expression of CTCF/CTCF-s on higher-order chromatin structures.
• Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells [ChIP-seq]
  GSE280302Homo sapiens11 个样本2026-10-31

  In this study, Biotin ChIP-seq was performed to obtain the independent genome binding sites of CTCF-s or CTCF. CTCF ChIP-seq was performed to investigate the influence of the overexpression of CTCF-s on the binding of CTCF in hESCs.
• Habitual betel nut chewing promotes oral squamous cell carcinoma tumorigenesis by inhibiting global methylation in normal oral mucosa
  GSE280233Homo sapiens33 个样本2026-10-31

  Oral squamous cell carcinoma (OSCC) is a major oral-maxillofacial tumor with marked effects on facial appearance and high recurrence rate. In addition to tobacco and alcohol consumption, betel nut chewing plays a significant role in promoting the occurrence of OSCC, highlighted by the prevalence of oral cancer in East Asia, Southeast Asia, and South Asia. However, the specific underlying mechanisms are unclear. By analyzing clinical data, we first noted that habitual betel nut chewing only affect occurrence of second primary tumors, indicated that it induces tumorigenic changes in the normal tumor-adjacent mucosa tissues. Tumorigenesis relies on the combined effect of genetic and environmental changes, with epigenetic changes, primarily methylation, serving as a key link connecting genetics and the environment. Herein, we analyzed global DNA methylation in the oral mucosa and found that habitual betel nut chewing leads to significant hypomethylation in the normal tumor-adjacent mucosa. This change makes the normal mucosa more similar to OSCC tissues than other normal tissues at the molecular pathological level. Our multiomics analysis revealed that habitual betel nut chewing may facilitate tumorigenesis by reducing the global DNA methylation level of normal mucosa, suppressing antitumor immunity, and promoting abnormal cell proliferation. Through experimental verification and screening, we identified five key genes involved in this process: DEPDC1B, ANLN, ECT2, SPC25, and PLK1. Our study revealed that habitual betel nut chewing can promote OSCC tumorigenesis by regulating global DNA methylation. Early detection of global DNA methylation and key gene markers may reveal potential targets for assessing OSCC risk.

  多组学
• Joint profiling of 5-methylcytosine, 5-hydroxymethylcytosine, and the transcriptome in single cells identifies factors responsible for genome-wide DNA methylation erasure in human primordial germ cell maturation
  GSE280112Homo sapiens23 个样本2026-10-31

  Reprogramming of DNA methylation plays a vital role in the establishment of cell identity during early mammalian development. To gain deeper mechanistic insights into this process requires capturing the entire dynamics of DNA methylation – both 5-methylcytosine (5mC) and its downstream oxidation product 5-hydroxymethylcytosine (5hmC) – in individual cells. Therefore, in this work, we report a new single-cell genome-wide strand-specific sequencing method, scMHT-seq, to jointly profile 5mC, 5hmC, and the transcriptome from individual cells. Using human embryonic stem cells (hESCs), we first show that scMHT-seq can accurately detect both 5mC and 5hmC from the same cell with minimal crosstalk in quantifying these two DNA modifications, and that the multi-modal measurements are in close agreement with individual measurements of 5mC and 5hmC in single cells. After establishing scMHT-seq, we next applied scMHT-seq to gain insights into human primordial germ cell (hPGC) maturation. After specification, hPGCs undergo rapid global demethylation as they mature, and this reprogramming is critical for normal development of gametes. However, it has not been possible to overcome this key epigenetic barrier in a dish, thereby limiting our ability to generate mature hPGC-like cells (hPGCLCs) and accomplish in vitro gametogenesis. To gain a deeper understanding of the molecular factors involved in germ cell maturation, we applied scMHT-seq to an extended in vitro culture system for generating hPGCLCs and observed partial and heterogeneous erasure of the methylome across single cells that is mechanistically predominantly driven by passive demethylation due to reduced DNMT1-mediated maintenance methylation activity. Notably, we discover that hPGCLCs in extended culture can be transcriptionally classified into two distinct states, with one population enriched for more mature hPGCLCs exhibiting genome-wide loss of the methylome. Moreover, we identify DND1 and SOX15 as two critical factors that are potentially key drivers of hPGCLC maturation. Overall, we demonstrate that scMHT-seq is a robust and high-throughput technology that can provide insights into the mechanisms driving DNA methylation dynamics and their effect on cellular states during hPGCLC maturation, thereby providing a platform to advance in vitro gametogenesis in humans.

  单细胞
• Chronic Inflammatory Responses in Diabetic Lung and its’ Implications for Tuberculosis Infection.
  GSE280089Mus musculus8 个样本2026-10-31

  Diabetes mellitus (DM) increases (~3.11-fold) the risk of tuberculosis (TB), leading to worse disease outcomes and higher relapse rates. scRNAseq revealed compromised adaptive and innate immunity in DM-TB mice, with decreased Th1 and M1 macrophage populations. Further analysis showed hyperinflammation in DM and dampened immune responses in DM-TB, marked by increased IL-16 signaling and reduced TNF and IFN-II responses.

  单细胞
• Type I regulatory T cells have overlapping phenotypes with circulating Tfh and Th1 in P. falciparum
  GSE279685Homo sapiens16 个样本2026-10-31

  Immunity to P. falciparum malaria develops slowly, requiring repeated infection in areas of high transmission, and wanes rapidly in the absence of parasite exposure. Key to this immunity, is the development of antibodies which is supported by CD4⁺ T follicular helper (Tfh) cells that drive robust germinal centre responses. However, in malaria, the malaria-specific CD4⁺ T cell compartment in peripheral blood is dominated by Type 1 regulatory T cells (Tr1), which produce high levels of IL-10 in response to parasites. Tr1-like Tfh cells (Tfh10) have been reported in several settings of repeated antigen stimulation but have not been investigated in malaria. Here we used single-cell RNA sequencing and multiparameter flow cytometry to characterise malaria-specific Tfh and Tr1 cells in a longitudinal cohort of highly exposed individuals and assessed their persistence after transmission interruption. Malaria-specific Tfh and Tr1 cells shared overlapping profiles, and Tr1 cell-like transcriptional signatures and phenotypes were detectable within the Tfh cell compartment. Tfh10 cell subsets were the dominant phenotype of malaria-specific Tfh cells. Following disruption of malaria transmission, the frequencies of malaria-specific Tr1 and Tfh10 cells declined. These findings highlight a close relationship between Tfh and Tr1 cells and show that the Tfh cell compartment in malaria is dominated by Tfh10 cells. The rapid waning of these cells in the absence of continuous exposure is consistent with requirements of persistent antigen in maintaining regulatory CD4 T cell phenotypes.

  单细胞
• Krüppel-like factor 5 remodels lipid metabolism in exercised skeletal muscle
  GSE279425Mus musculus16 个样本2026-10-31

  Regular physical activity induces a variety of health benefits, preventing and counteracting diseases caused by a sedentary lifestyle. However, the molecular underpinnings of skeletal muscle plasticity in exercise remain poorly understood. We identified a role of the Krüppel-Like Factor 5 (Klf5) in this process, in particular in the regulation of lipid homeostasis. Surprisingly, gain- and loss-of-function studies in muscle in vivo revealed seemingly opposite functions of Klf5 in the response to an acute exercise bout and chronic training, modulating lipid oxidation and synthesis, respectively. Thus, even though only transiently induced, the function of Klf5 is complex and integral for a normal long-term training response. These findings highlight the importance of this mediator of external stress response to adaptive remodeling of skeletal muscle tissue.
• Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue
  GSE276213Mus musculus; Homo sapiens22 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

  空间转录组SuperSeries
• Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue [DNA-Seq]
  GSE276212Homo sapiens; Mus musculus11 个样本2026-10-31

  Tumor heterogeneity arises from the sequential acquisition of somatic mutations and the selection of fitter clones, leading to distinct genotypes and phenotypes. Joint mapping of genome and transcriptome in the same tumor tissue can directly link clonoal relation to transcriptional state enabling a more in-depth understanding of intrinsic and extrinct tumor heterogeneity in the tissue context. Here, we introduce Spatial-GT-seq, a spatial multi-omic technology capable of genome-wide co-profiling of the genome and transcriptome at near single-cell resolution. We demonstrated in situ identification of tumor subclones in a mouse model of lung metastasis, with parallel transcriptomic profiles indicating that the gene expression profile of the same tumor clone is altered by the tumor microenvironment. Furthermore, analysis of primary and recurrent human pancreatic neuroendocrine tumors reveals both persistent and newly emerging tumor subclones, exhibiting transcriptional changes in both the original and recurrence sites. These findings highlight Spatial-GT-seq as a valuable platform for studying genotype-phenotype-microenvironment associations, providing new insights into cancer evolution and heterogeneity.

  单细胞空间转录组多组学
• Spatial genome and transcriptome co-mapping reveals clonal heterogeneity in tumor tissue [RNA-Seq]
  GSE276211Homo sapiens; Mus musculus11 个样本2026-10-31

  Tumor heterogeneity arises from the sequential acquisition of somatic mutations and the selection of fitter clones, leading to distinct genotypes and phenotypes. Joint mapping of genome and transcriptome in the same tumor tissue can directly link clonoal relation to transcriptional state enabling a more in-depth understanding of intrinsic and extrinct tumor heterogeneity in the tissue context. Here, we introduce Spatial-GT-seq, a spatial multi-omic technology capable of genome-wide co-profiling of the genome and transcriptome at near single-cell resolution. We demonstrated in situ identification of tumor subclones in a mouse model of lung metastasis, with parallel transcriptomic profiles indicating that the gene expression profile of the same tumor clone is altered by the tumor microenvironment. Furthermore, analysis of primary and recurrent human pancreatic neuroendocrine tumors reveals both persistent and newly emerging tumor subclones, exhibiting transcriptional changes in both the original and recurrence sites. These findings highlight Spatial-GT-seq as a valuable platform for studying genotype-phenotype-microenvironment associations, providing new insights into cancer evolution and heterogeneity.

  单细胞空间转录组多组学
• Collection of CRC cell line grown in vitro
  GSE271191Homo sapiens19 个样本2026-10-31

  Recent studies revealed the presence of an aggressive subgroup of colorectal cancer (CRC) that exhibits a distinct tumor growth pattern, characterized by high abundance of cancer-associated fibroblasts (CAFs). To identify cancer cells-intrinsic traits underlie this phenotype and to characterize its stromal features, we generated mouse xenografts from 19 CRC cell lines, where normal mouse stroma cells are recruited and educated by epithelial cancer cells. The in vivo xenograft growth rate showed high variability between cell lines, revealing a subgroup of slow-paced tumors. Cancer cells of this subgroup display distinctive transcriptional features, only partially captured by previously described CRC molecular subtypes, involving epithelial-mesenchymal transition and cooperation with a specific CAF population in remodeling the extracellular matrix. We therefore called the cancer cell signature “epithelial matrix remodeling” (EMR), and the CAF signature “matrix remodeling CAF” (mrCAF). In pan-cancer analysis, the EMR and mrCAF signatures were co-detected and associated with poor prognosis in multiple tumor types. Altogether, these results highlight the intrinsic capability of cancer cells to recruit, educate and cooperate with CAFs, indicating route toward tumor progression involving the interaction between tumor and its microenvironment.
• Collection of CRC cell line grown in vivo
  GSE267353Homo sapiens38 个样本2026-10-31

  Recent studies revealed the presence of an aggressive subgroup of colorectal cancer (CRC) that exhibits a distinct tumor growth pattern, characterized by high abundance of cancer-associated fibroblasts (CAFs). To identify cancer cells-intrinsic traits underlie this phenotype and to characterize its stromal features, we generated mouse xenografts from 19 CRC cell lines, where normal mouse stroma cells are recruited and educated by epithelial cancer cells. The in vivo xenograft growth rate showed high variability between cell lines, revealing a subgroup of slow-paced tumors. Cancer cells of this subgroup display distinctive transcriptional features, only partially captured by previously described CRC molecular subtypes, involving epithelial-mesenchymal transition and cooperation with a specific CAF population in remodeling the extracellular matrix. We therefore called the cancer cell signature “epithelial matrix remodeling” (EMR), and the CAF signature “matrix remodeling CAF” (mrCAF). In pan-cancer analysis, the EMR and mrCAF signatures were co-detected and associated with poor prognosis in multiple tumor types. Altogether, these results highlight the intrinsic capability of cancer cells to recruit, educate and cooperate with CAFs, indicating route toward tumor progression involving the interaction between tumor and its microenvironment.
• TAF1-dependent transcriptional dysregulation underlies multiple sclerosis
  GSE255578Mus musculus12 个样本2026-10-31

  In the search for new targets for therapeutic intervention, MS-associated common variants provide clues about etiology-relevant molecular mechanisms, but the individual effect of each variant is minimal. A current priority to better understand the molecular basis of MS and to identify targets for designing progression-modifying therapies, is therefore to detect in the CNS of MS patients specific biochemical alterations -likely related to environmental factors and/or GWAS-identified molecular mechanisms- that per se would suffice to cause MS progression.
• Transcriptomic changes from resulting from treatment of KNS42 with drugs of abuse
  GSE246989Homo sapiens28 个样本2026-10-31

  KNS42 cells were treated with drugs of abuse (ethanol, cocaine, morphine, THC, and psilocin) prior to RNA sequencing. A bioinformatics pipeline of Trim Galore, Kallisto, DESeq2 and Qiagen Ingenuity Pathway Analysis was used for pathway analysis.
• Deciphering the interaction between Twist1 and PPARγ during adipocyte differentiation
  GSE246718Mus musculus12 个样本2026-10-31

  Obesity, a worldwide epidemic in recent years, is mainly due to the uncontrolled development of adipose tissues, which includes adipocyte hypertrophy and hyperplasia. Adipocyte differentiation is a process involving multiple transcription factor cascades, and the exact mechanism has not yet been defined. As a bHLH transcription factor, Twist1 exerts its activity by forming homo- or heterodimers with other factors. In this study, we showed Twist1 restricts adipogenesis through PPARγ. Expression of various differentiation markers (including PPARγ and adiponectin) and triglyceride-containing lipid droplets were decreased with overexpression of Twist1. Pathway enrichment analysis of RNA-seq data showed that differentially expressed genes (DEGs) caused by Twist1 overexpression were significantly related to lipolysis and PPARγ signaling. This implicates that Twist1 plays important regulatory roles in these processes. ChIP and dual luciferase assays showed that Twist1 could bind either PPARγ or adiponectin promoter to repress their respective transcription or directly to PPARγ protein to regulate its transcriptional activity. Furthermore, Twist1 directly interacted RXRα, which usually forms heterodimer with PPARγ to regulate adipogenesis. Taken together, our results suggest that Twist1 is an inhibitory modulator of adipogenesis and its function is likely through direct interaction with PPARγ protein or its gene promoter.