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。

• Effect of PRAME overexpression on gene expression of A549 NSCLC cells
  GSE292191Homo sapiens4 个样本2026-10-28

  To investigate the function of PRAME in lung cancer, we established OE PRAME A549 cell line.
• Muscles transcriptomic response to exercise
  GSE287162Mus musculus12 个样本2026-10-28

  The main goal of study was to see the transcriptional response to acute exercise in mice . For this the RNA seq was done in WT rest and WT exercise. We then want to reproduce the same result in HDAC3 ko mice and found the same result. Tissues were harvested immediately after the last session. RNA-seq identified that most differentially expressed genes (DEGs, exercise vs. rest) were upregulated upon exercise. We observed similar results in wild-type (WT) mice comparing exercise vs. rest and found that exercise-induced activation is independent of HDAC3, supporting the rationale for our investigation and demonstrate the robustness and reproducibility of the results that exercise-induced activation of our target gene is independent of HDAC3
• RNA-seq analysis after venetoclax and azacitidine treatment in AML cells
  GSE284469Homo sapiens18 个样本2026-10-28

  RNA-seq analysis was performed in three isogenic MOLM-13 acute myeloid leukemia (AML) cell lines (p53 WT/p53 R248Q/p53 KO) to analyze gene expression changes after treatment with venetoclax and azacitidine.
• Lipid nanoparticle-mediated TFEB mRNA delivering for treatment of non-alcoholic fatty liver disease
  GSE283076Mus musculus16 个样本2026-10-28

  Non-alcoholic fatty liver disease (NAFLD) is a disease characterized by excessive lipid accumulation in the liver, often accompanied by obesity and insulin resistance. As the disease progresses, it can lead to non-alcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and even hepatocellular carcinoma. The excessive activation of the mTORC1 complex promotes TFEB phosphorylation, thereby suppressing the TFEB-dependent lysosomal autophagy pathway and contributing to the development of NAFLD. Therefore, pharmacological activation of TFEB may offer a potential therapeutic strategy for NAFLD. However, currently, there is no drug that can directly activate TFEB. While mTORC1 inhibitors can indirectly activate TFEB, their use is limited by systemic side effects. In this study, we utilized lipid nanoparticles (LNP) to deliver TFEB mRNA to the liver. This targeted approach enhanced TFEB expression in hepatic cells, promoted autophagy, and mitigated NAFLD progression in a murine model.
• OMP38 of carbapenem-resistant Acinetobacter baumannii-mediated mtDNA release activates the cGAS-STING signalling to induce inflammatory response
  GSE280491Mus musculus5 个样本2026-10-28

  Carbapenem-resistant Acinetobacter baumannii (CRAB) has become a major threat in the treatment of bacterial infection, and immunotherapy in a non-antibiotic-dependent manner is an effective way to overcome CRAB infection. However, the role of the innate immune response in CRAB infection is poorly understood. Here, we reported that CRAB infection induced a cytosolic DNA-sensing signalling pathway and significant IFN-β production in mice post CRAB infection. The knockout of STING reduced bacterial burden, the production of inflammatory cytokines and lung injury in mice post CRAB infection. The cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS) and the adaptor protein stimulator of interferon genes (STING) were required for CRAB-induced IFN-β expression in macrophages. Intriguingly, CRAB utilized outer membrane vesicles (OMVs) to transport outer membrane protein 38 (OMP38) into mitochondria, triggering mitochondrial DNA (mtDNA) release into the cytosol through the mitochondrial permeability transition pore (mPTP) and activating the cGAS-STING signalling. Finally, epigallocatechin gallate (EGCG) was demonstrated to block the activation of the cGAS-STING pathway and ameliorate CRAB-induced excessive inflammatory response. These results demonstrated that the early innate immune response to CRAB infection was activated in a cGAS-STING-dependent manner, which could be a potential therapeutic target for CRAB infection.
• Effect of YAP and KLF4 overexpression on gene expression of cerebral microvascular endothelial cells [RNA-Seq]
  GSE280201Mus musculus12 个样本2026-10-28

  Our preliminary findings revealed that YAP acts with KLF4. We here report overexpression of YAP and KLF4, either individually or in combination, led to significant changes in the transcriptomic profiles. YAP and KLF4 have substantial overlaps on co-regulation gene, which has a potential synergistic effect on gene expression. Our findings suggest that the co-regulated DEGs play pivotal roles in vascular and cellular processes, highlighting the synergistic effects of YAP and KLF4 on these biological activities.
• CCM2 knockout promotes transcriptional activity of YAP and KLF4 [CUT&Tag]
  GSE280200Mus musculus12 个样本2026-10-28

  CCM2 knockout dramatically increased the number of KLF4 regulatory genes, and similarly, the number of YAP regulatory genes surged. Consistently, the number of genes co-regulated by KLF4 and YAP also increased after CCM2 loss. Upon performing functional analyses of the genes co-regulated by KLF4 and YAP, we found that the genes in WT primary MBMECs were unable to enrich specific signaling pathways, while the genes in Ccm2-knockout primary MBMECs were enriched in several pathways, including SMAD binding, Rho GTPase binding, kinase regulator activity, et al
• Unveiling the role of UPF1-mediated mRNA decay in melanoma tumorigenesis by modulating the miR-101-3p/NANOS1 axis
  GSE267965Homo sapiens20 个样本2026-10-28

  Numerous studies have reported that Up-frameshift protein 1 (UPF1) as a crucial posttranscriptional regulator in nonsense-mediated mRNA decay (NMD), attributing its role to tumorigenesis across various cancers. However, its recently unveiled function in UPF1-mediated mRNA decay (UMD), intricately coordinated with miRNA, remains unexplored in the context of tumorigenesis. Herein, we elucidate the pivotal role of UPF1 in governing melanoma tumorigenesis by modulation of NANOS1 expression via miR-101-3p. Depletion of UPF1 across three melanoma cell lines significantly impaired cell growth, migration, and invasion by cell cycle arrest and disrupted tumor formation in vivo. Through comprehensive RNA-seq and biochemical analyses, we elucidate that attenuation of UPF1 leads to an increase in NANOS1 expression, consequently suppressing melanoma tumorigenesis. Mechanistically, UPF1 orchestrates the destabilization of NANOS1 via UPF1-mediated mRNA decay (UMD) facilitated by miR-101-3p. Intriguingly, our findings highlight a novel protein modification event involving the phosphorylation of ELK1 by the UPF1/miR-101-3p/NANOS1 pathway, as revealed by antibody microarray analysis. Importantly, our study underscores the significance of UPF1 and NANOS1 in regulating melanoma tumorigenesis, even in drug-resistant cell lines and in vivo models including syngeneic and xenograft mouse models. Collectively, these insights shed light on the role of UMD in melanoma tumorigenesis through the UPF1/NANOS1/miR-101-3p axis and unveil potential therapeutic strategies for both primary and drug-resistant melanoma treatment.
• Filamin B, a novel RNA-binding protein, extensively regulates the expression and alternative splicing of genes associated with osteoblast development in MC3T3-E1 cells
  GSE246668Mus musculus6 个样本2026-10-28

  Filamin B (FLNB) encodes an actin-binding protein and also acts as a novel RNA-binding protein involved in cell movement and signal transduction, playing a crucial role in bone growth. However, the impact of dysregulated FLNB expression on the molecular level in the skeletal system remain unknown. In this study, stably transfected MC3T3-E1 cell lines with FLNB knockdown were constructed to investigate the regulatory mode of FLNB in the molecular level of osteoblasts by RNA-seq sequencing. Functionality experiments revealed that FLNB knockdown led to decreased proliferation, migration, and differentiation of MC3T3-E1 cells compared to the empty vector group. In addition, differentially expressed genes (DEGs) and results showed that FLNB was mainly enriched in the expression of genes related to osteoblast proliferation, differentiation and migration, such as ITGA10, Cebpβ, Grem1, etc. Alternative splicing (AS) results observed significant changes in Tpx2 and Evc related to skeletal development.According to the current study, we conducted the first investigation into the transcriptomic and alternative splicing level of FLNB in pre-osteoblast to analyze its regulatory function in bone growth and development. This study lays the foundation for the current insights into the mechanisms of gene regulation mediated by FLNB during skeletal development.
• Overexpression of desmin and vimentin in primary human bladder smooth muscle cells
  GSE127725Homo sapiens9 个样本2026-10-28

  Desmin and Vimentin overexpression differentially regulates smooth muscle gene expression in primary human bladder smooth muscle (HBSM) cells
• Detailed characterization of the immune response to Epstein-Barr virus in multiple sclerosis and following B cell depleting treatment
  GSE352228Homo sapiens24 个样本2026-10-27

  B-cell-depleting therapies are increasingly used for the treatment of multiple sclerosis (MS). Here, we characterize the impact of BCDT on humoral and cellular immune response to Epstein-Barr virus (EBV) in persons with MS (pwMS). We find that EBV viral load does not differ between pwMS and HC. By contrast, distinct differences are found in both humoral and cellular EBV-specific immunity in MS. EBV-specific antibody titres are increased in pwMS, whereas cellular immunity diverges toward lower CD8+ T cell reactivity against lytic antigens, including BZLF1. Notably, during periods of disease activity, both CD4+ and CD8+ T cell responses to lytic antigens tend to be higher. In addition, BZLF1-specific T cell clones recognizing the peptide RAKFKQLL were the most clonally expanded population in the intrathecal compartment of a pwMS with high CSF T cell counts. BCDT reduces EBV viral load and is associated with pronounced reduction in CD8+ T cell responses to all lytic EBV antigens. These findings delineate distinct alterations in EBV-specific immunity in MS and demonstrate that BCDT modulates both viral load and T cell responses. The data support a potential role for CD8+ T cell clones targeting lytic EBV proteins in MS pathogenesis.
• Transcriptome-wide mapping reveals an RNA-dependent mechanism of platinum cancer drugs. [ptRNAseq_A2780_Fractionation]
  GSE352212Homo sapiens24 个样本2026-10-27

  Clinically used small molecules have been predicted to off-target to RNAs. However, the extent of this interaction is small molecule cancer therapeutics have not been characterized. Here, we screened for anticancer small molecules for their RNA interactions and uncovered widespread RNA off-targeting. Cisplatin was found to be one among the RNA binders. We used it as a model agent to identify the specific transcripts it interacts with. To accomplish this, we developed Plat-RNAseq, a click-chemistry-mediated transcriptome-wide assay. Our results revealed that cisplatin binding was enriched at guanine-rich regions capable of forming RNA G-quadruplexes (rG4s). We found that the recruitment of cisplatin to rG4s partially contributed to its cytotoxicity, revealing a noncanonical mechanism of action for this widely used chemotherapeutic agent. This experiment applied PlatRNA-seq to chromatin-associated, nuclear and cytoplasmic RNA fractions to assess whether platinum binding occurs co-transcriptionally or on mature RNA.
• Transcriptome-wide mapping reveals an RNA-dependent mechanism of platinum cancer drugs. [ChIP-Seq_Spike-In]
  GSE352210Homo sapiens6 个样本2026-10-27

  Clinically used small molecules has been predicted to off-target to RNAs. However, the extend of this interaction is small molecule cancer therapeutics has not been characterized. Here, we screened for anticancer smalll molecules for their RNA interactions and uncovered widespread RNA off-targeting. Cisplatin was found to be one among the RNA binders. We used it as a model agent to identify the specific transcripts it interact with. To accomplish this, we developed Plat-RNAseq, a click-chemistry-mediated transcriptome-wide assay. Our results revealed that cisplatin binding was enriched at guanine-rich regions capable of forming RNA G-quadruplexes (rG4s) .We found that the recruitment of cisplatin to rG4s partially contributed to its cytotoxicity, revealing a noncanonical mechanism of action for this widely used chemotherapeutic agent. To assess the prevalence of RNA Pol II stalling in the cisplatin-target RNA we used RNA Pol II ChIP-seq and caculated the genome-wide stalling. This experiment uses RNA Pol II ChIP-seq with a Drosophila chromatin spike-in for quantitative normalization, unlike the previously deposited Pol II ChIP-seq (GSE309934), which was normalized to library size without a spike-in.
• GRHL2 loss alters redox homeostasis and attenuates erastin-induced ferroptosis in colorectal cancer cells
  GSE352117Homo sapiens6 个样本2026-10-27

  Redox homeostasis critically determines ferroptosis sensitivity, but the role of grainyhead-like 2 (GRHL2) in colorectal cancer remains unclear. RNA sequencing was performed to compare parental HCT116 cells with a CRISPR/Cas9-generated B8 GRHL2-KO clone and to define GRHL2-associated transcriptional changes relevant to redox homeostasis and ferroptosis sensitivity.
• Transcriptomic analysis of mucosal immunity in mouse lung tissues induced by sequential Sad23L-RSV vaccination
  GSE352070Mus musculus15 个样本2026-10-27

  We performed transcriptomic analysis of lung tissues from BALB/c mice vaccinated with a novel adenovirus-vectored RSV vaccine (Sad23L-RSV) via an intranasal prime/intramuscular boost regimen. Lung tissues were collected at days 0, 2, 7, and 28 after the booster immunization to investigate the molecular mechanisms of durable mucosal immunity.
• Micro-C-TALE: BAC-based targeted high-resolution measurement of 3D chromatin interactions [Micro-C-TALE]
  GSE351910Homo sapiens2 个样本2026-10-27

  Chromosome conformation capture methods have greatly advanced our understanding of genome organization, but obtaining high-resolution interaction maps of selected genomic regions remains costly due to the sequencing requirements. Here, we introduce Micro-C-TALE, a new chromosome conformation capture method that combines Micro-C, which uses micrococcal nuclease to the resolution and sensitivity of chromatin interaction measurements, and C-TALE, which uses probes generated from bacterial artificial chromosomes (BACs) for targeted enrichment. This combination enables the generation of high-resolution interaction maps without requiring custom synthesis of capture oligonucleotides. We applied Micro-C-TALE to a 214 kb region in human HAP1 cells, obtaining detailed interaction maps with approximately ~5-6 million sequenced read pairs. Compared with published genome-wide Micro-C data, Micro-C-TALE yielded a higher amount of informative interactions within the targeted region despite ~550-fold lower sequencing depth. To evaluate the sensitivity of the method to fine-scale changes in genome organization, we introduced a CTCF binding site into the targeted region using CRISPR-Cas9. Comparing Micro-C-TALE to the restriction enzyme-based C-TALE, we found Micro-C yielded a ~5-fold higher fraction of informative reads and detected novel CTCF-mediated point interactions associated with the inserted CTCF site, which were barely discernible using C-TALE. Our results demonstrate that Micro-C-TALE provides a flexible and cost-effective approach for targeted high-resolution measurement of chromatin interactions, facilitating the investigation of fine-scale genome organization and its response to genetic perturbations.

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• Micro-C-TALE: BAC-based targeted high-resolution measurement of 3D chromatin interactions [C-TALE]
  GSE351909Homo sapiens1 个样本2026-10-27

  Chromosome conformation capture methods have greatly advanced our understanding of genome organization, but obtaining high-resolution interaction maps of selected genomic regions remains costly due to the sequencing requirements. Here, we introduce Micro-C-TALE, a new chromosome conformation capture method that combines Micro-C, which uses micrococcal nuclease to the resolution and sensitivity of chromatin interaction measurements, and C-TALE, which uses probes generated from bacterial artificial chromosomes (BACs) for targeted enrichment. This combination enables the generation of high-resolution interaction maps without requiring custom synthesis of capture oligonucleotides. We applied Micro-C-TALE to a 214 kb region in human HAP1 cells, obtaining detailed interaction maps with approximately ~5-6 million sequenced read pairs. Compared with published genome-wide Micro-C data, Micro-C-TALE yielded a higher amount of informative interactions within the targeted region despite ~550-fold lower sequencing depth. To evaluate the sensitivity of the method to fine-scale changes in genome organization, we introduced a CTCF binding site into the targeted region using CRISPR-Cas9. Comparing Micro-C-TALE to the restriction enzyme-based C-TALE, we found Micro-C yielded a ~5-fold higher fraction of informative reads and detected novel CTCF-mediated point interactions associated with the inserted CTCF site, which were barely discernible using C-TALE. Our results demonstrate that Micro-C-TALE provides a flexible and cost-effective approach for targeted high-resolution measurement of chromatin interactions, facilitating the investigation of fine-scale genome organization and its response to genetic perturbations.

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• SB89: A Murine Dermis-Derived Macrophage Cell Line for Studies of Skin Immune Responses
  GSE351881Mus musculus6 个样本2026-10-27

  Resident dermal macrophages (DMs) play essential roles in maintaining skin homeostasis and initiating inflammatory responses during tissue injury and against infectious agents. However, studies of their cellular mechanisms have been limited by their low abundance in steady-state skin and by technical challenges in isolating resident DMs. Here, we describe the generation and characterization of a novel DM cell line, termed SB89. F4/80+ skin-resident DMs were sorted and immortalized using J2 retroviral transduction. SB89 cells display a stable, homogeneous macrophage phenotype and distinct surface markers compared with Langerhans cells and alveolar macrophages. Functionally, SB89 cells efficiently phagocytose methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, zymosan particles, and apoptotic cells, and effectively kill MRSA. Importantly, SB89 cells respond to LPS, as evidenced by production of IL-6, TNF, and Nos2, and by MRSA-induced production of inflammatory cytokines, chemokines, and eicosanoids. Importantly, SB89 cells are genetically tractable and amenable to genetic manipulation, supporting efficient miRNA gene silencing via RNAi and gene introduction via plasmid-based gene expression transfection. Bulk RNA-seq analysis revealed that SB89 cells are transcriptionally distinct from immortalized bone marrow-derived macrophages and are enriched for pathways associated with innate immune responses, chemotaxis, cell adhesion, and GPCR signaling. Together, these findings establish SB89 as a renewable, genetically tractable dermis-derived macrophage model that can support reproducible studies of skin-associated macrophage functions. This cell line represents a powerful platform for mechanistic, genetic, and translational studies in skin immunobiology.
• Spatial transcriptomic profiling of human left ventricular tissue in ischaemic heart disease and dilated cardiomyopathy
  GSE351778Homo sapiens2 个样本2026-10-27

  Spatially resolved single-cell gene expression profiling was performed on fresh-frozen human left ventricular tissue from one ischaemic heart disease (IHD) and one dilated cardiomyopathy (DCM) specimen. The Xenium Human Multi-Tissue and Cancer Gene Expression panel supplemented with 100 custom probes was used to characterise cardiomyocytes and cardiac fibroblasts and investigate spatial relationships between fibroblast subpopulations and cardiomyocyte.

  单细胞空间转录组
• Adipose mitochondrial functional enhancement via DsbA-L rewires systemic aging through an adipokine-mediated longevity pathway
  GSE351767Mus musculus4 个样本2026-10-27

  Mitochondrial dysfunction is a hallmark of aging, but whether restoring mitochondrial function in adipose tissue alone can delay systemic aging is unknown. Here we show that adipose-specific upregulation of the mitochondrial chaperone DsbA-L in mice improves metabolic and cognitive function and extends lifespan, linking adipose mitochondrial fitness directly to systemic aging. DsbA-L upregulation reprograms adipose gene expression and raises circulating levels of the adipokine Serpina3m. Fat-body-specific knockdown of Spn42De (CG9460), the Drosophila serpin counterpart of Serpina3m, shortens lifespan, whereas its overexpression extends it. SERPINA3, the human ortholog, is enriched in centenarians. Unlike conventional mitochondrial enhancers, DsbA-L couples metabolic efficiency to endocrine signaling, and berberine increases DsbA-L expression, indicating that this pathway is pharmacologically tractable. These benefits occur in both sexes and identify DsbA-L–Serpina3m signaling as a target for healthy aging.
• Transcriptomics of human fetal microglia infected with HIV-1
  GSE351613Homo sapiens36 个样本2026-10-27

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Transcriptomics of human fetal microglia infected with HIV-1 [V8 RNA-Seq]
  GSE351612Homo sapiens12 个样本2026-10-27

  Microglia act as HIV reservoirs in the brain and contribute to the development of HIV-associated neurocognitive disorders. Understanding the pathobiology of HIV-infected microglia is therefore essential. Here, we examined the transcriptome of primary microglia infected ex vivo with HIV-1. Analyses reveal a significant expression modulation of DNA/cell cycle, cellular stress-related, as well as non-membrane bounded organelle assembly-related genes, and a broad effect on microRNA expression. MicroRNA-23b is identified among upregulated microRNAs in HIV-1-infected microglia, and the downregulated g3bp2 mRNA validated as its target. G3BP2 is a component of stress granules (SGs), which serve as antiviral and proinflammatory platforms. MicroRNA-23b mimics reduce both SG assembly and G3BP2 expression in arsenite (As)-treated monocyte-derived microglial cells (MDMi), and few SGs aggregate in infected MDMi in response to As-mediated stress. MicroRNA-23b inhibitors partially re-establish SG formation and reduce HIV-1 replication and spread. Thus, microRNA-23b induction enables HIV-1 to counter SG assembly in infected microglia, a host response that restricts HIV-1 replication and ensuing neuropathogenesis
• Transcriptomics of human fetal microglia infected with HIV-1 [V6 miRNA-Seq]
  GSE351611Homo sapiens24 个样本2026-10-27

  Microglia act as HIV reservoirs in the brain and contribute to the development of HIV-associated neurocognitive disorders. Understanding the pathobiology of HIV-infected microglia is therefore essential. Here, we examined the transcriptome of primary microglia infected ex vivo with HIV-1. Analyses reveal a significant expression modulation of DNA/cell cycle, cellular stress-related, as well as non-membrane bounded organelle assembly-related genes, and a broad effect on microRNA expression. MicroRNA-23b is identified among upregulated microRNAs in HIV-1-infected microglia, and the downregulated g3bp2 mRNA validated as its target. G3BP2 is a component of stress granules (SGs), which serve as antiviral and proinflammatory platforms. MicroRNA-23b mimics reduce both SG assembly and G3BP2 expression in arsenite (As)-treated monocyte-derived microglial cells (MDMi), and few SGs aggregate in infected MDMi in response to As-mediated stress. MicroRNA-23b inhibitors partially re-establish SG formation and reduce HIV-1 replication and spread. Thus, microRNA-23b induction enables HIV-1 to counter SG assembly in infected microglia, a host response that restricts HIV-1 replication and ensuing neuropathogenesis
• Transcriptomic profiling of mouse bone marrow neutrophils treated with Propionibacterium acnes with or without human umbilical cord blood mesenchymal stem cell-derived exosomes
  GSE351531Mus musculus8 个样本2026-10-27

  This study investigates transcriptional responses of mouse bone marrow neutrophils to human umbilical cord blood mesenchymal stem cell-derived exosomes during Propionibacterium acnes stimulation. Bulk RNA sequencing was performed on neutrophils exposed to P. acnes alone or to P. acnes together with exosomes. The dataset comprises eight samples and includes paired-end sequencing reads, gene-level read counts, and FPKM expression values. It supports investigation of inflammatory responses and pathways associated with neutrophil extracellular trap formation.
• Synapse-seq reveals cytotoxic CD4+ T cell suppression of human antibody responses
  GSE351507Homo sapiens22 个样本2026-10-27

  Deciphering the molecular dialogue between cells is central to understanding how immune responses are orchestrated. Here we applied Synapse‐seq, a new image‐enabled cell interaction sorting and transcriptomic profiling approach, to characterize CD4+ T-B cell synaptic interactions in human spleen organoids. We identified B cells synapsing with FOXP3+ regulatory T cells (Tregs) expressing high levels of perforin and granzymes A and B, indicating that cytotoxicity is a major mechanism of CD4+ Treg suppression of specific B cells. Antigen-specific Synapse-seq revealed opposing phenotypes of viral and autoreactive T-B interactions and identified a hemagglutinin-specific TCR-BCR pair in a human immune system. Both CD3+ and CD4+ T cell-specific knockouts of cytotoxic genes robustly increased antibody responses against both nuclear autoantigens and viral antigens. Consistent with these findings, patients with systemic lupus erythematosus (SLE) exhibited a significant enrichment of cytotoxic CD4+ Tregs. Our findings support cytotoxicity as a dominant way CD4+ T cells regulate B cells and antibody responses. More broadly, we suggest Synapse-seq as a generalizable method to characterize cell interactions without requiring cell engineering.
• Study of LETT@MVs‑induced ferroptosis in tumor cells via supplementation of PUFA
  GSE351467Homo sapiens4 个样本2026-10-27

  Ferroptosis represents a promising therapeutic strategy for cancer, yet its anti‑tumor efficacy is largely limited by insufficient polyunsaturated fatty acids (PUFA) within the tumor microenvironment (TME). Aloe vera thylakoid membranes, naturally rich in PUFA, are an ideal source to facilitate robust lipid peroxidation. To address biological delivery obstacles, we constructed tumor‑targeting biomimetic microvesicles (LETT@MVs) by engineering aloe‑thylakoid‑derived microvesicles (TDMVs) with the multifunctional peptide LETT, which enables tumor‑targeted delivery and lysosomal escape. We systematically characterized the influences of LETT@MVs on hepatocellular carcinoma (HCC) cells, including cell viability, vasculogenic mimicry (VM) formation, lipid peroxidation and ferroptosis in vitro. Antitumor potency and biosafety were further validated using an orthotopic HCC mouse model. Mechanistically, multi‑omics strategies combining bulk RNA‑seq, metabolomics and scRNA‑seq were applied to decipher underlying molecular events. LETT@MVs were effectively internalized by HCC cells and successfully escaped lysosomal degradation. Taking advantage of endogenous PUFA stored in thylakoid components, LETT@MVs triggered potent lipid peroxidation and ferroptosis, meanwhile remodelled the extracellular matrix (ECM) to suppress vasculogenic mimicry. In orthotopic HCC mice, LETT@MVs markedly retarded tumor growth via ferroptosis induction and VM repression without obvious safety risks. Integrated multi‑omics data demonstrated that LETT@MVs rewired transcriptional and metabolic profiles of HCC cells, driving highly‑metabolic tumor cells toward ferroptotic stress status and generating near‑death cell subpopulations. Collectively, our work validates that aloe‑thylakoid‑originated biomimetic nanoplatform can trigger robust tumor ferroptosis through PUFA supplementation, providing new clues to conquer ferroptosis resistance and advance therapeutic interventions for hyper‑metabolic tumors.

  单细胞
• Genomic and Immune Profiling Characterizes Immune Heterogeneity and a TIGIT-Associated Subtype in Intrahepatic Cholangiocarcinoma
  GSE350183Homo sapiens164 个样本2026-10-27

  Background and Aims: Intrahepatic cholangiocarcinoma (iCCA) is characterised by marked molecular and microenvironmental heterogeneity and moderate response to immunotherapy. We aimed to define the genomic and spatial determinants of immune checkpoint activity in iCCA and their association with clinical outcome. Approach and Results: We performed integrated transcriptomic, DNA panel sequencing, and multiplex immunohistochemistry analyses in a cohort of 144 patients with iCCA. Tumors were classified according to STIM-defined microenvironmental subtypes. Spatially resolved immune profiling was conducted across tumor core, stroma, invasive margin, and adjacent liver. Immune checkpoint expression, cellular proximity, and clinical outcome were analysed using Cox regression and Kaplan-Meier methods. TIGIThigh tumors were further characterised by differential gene expression and pathway enrichment analyses. STIM classification stratified tumors into inflamed (47%) and non-inflamed (53%) subtypes with distinct survival outcomes and genomic profiles. Recurrent alterations in CDKN2A/B, TP53, MTAP, and BAP1 showed subtype-specific enrichment and prognostic relevance. Spatial immune profiling revealed compartment-specific distributions of T cells and immune checkpoints, with predominance of TIGIT and PD-1 expression in stromal and marginal regions. Most tumor-infiltrating T cells lacked inhibitory receptor expression, while co-expression of multiple checkpoints was uncommon. TIGIThigh tumors displayed coordinated activation of immune effector, antigen presentation, and interferon signalling pathways, alongside enrichment of distinct genomic alterations, defining an immune-activated molecular subtype. Conclusions: Integrated genomic and spatial immune profiling reveals pronounced context-dependent heterogeneity of immune checkpoint regulation in iCCA. TIGIT delineates an immune-activated subtype with distinct molecular features, providing a potential biomarker framework for patient stratification and rational immunotherapeutic targeting.

  空间转录组
• TSC2-Mutant Yucatan Minipig Cardiac Rhabdomyoma Model Reveals mTORC1 Activation and MITF/TFE Expression Signature
  GSE349392Sus scrofa; Homo sapiens18 个样本2026-10-27

  Tuberous sclerosis complex (TSC) is an inherited tumor predisposition syndrome caused by pathogenic variants in TSC1 or TSC2. We generated a heterozygous TSC2-mutant Yucatan minipig carrying the recurrent pathogenic TSC2 p.Arg505* variant and characterized its cardiac phenotype using histopathology, immunohistochemistry, and RNA sequencing. TSC2-mutant minipigs developed multiple cardiac rhabdomyomas resembling human lesions. Comparative transcriptomic analyses identified a conserved TSC-associated expression program and MITF/TFE-regulated lysosomal pathways in human and minipig tumors.
• Genome-wide CRISPRi-seq profiling of essential-gene contributions to aminoglycoside susceptibility in Pseudomonas aeruginosa PAO1
  GSE349013Pseudomonas aeruginosa40 个样本2026-10-27

  This CRISPRi-seq dataset quantifies the abundance of 83,078 sgRNAs in a pooled Pseudomonas aeruginosa PAO1 CRISPRi library across untreated, aminoglycoside-treated and serum-containing conditions. Four independent experimental batches were used to measure untreated fitness, responses to tobramycin or amikacin, and fitness in 60% fetal bovine serum. The deposited processed data include raw guide counts and complete guide- and gene-level results for the predefined comparisons used in the study.

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• RNA-seq analysis of CRISPRi-mediated gene silencing and tobramycin response in Pseudomonas aeruginosa PAO1
  GSE349001Pseudomonas aeruginosa18 个样本2026-10-27

  This RNA-seq dataset profiles transcriptional responses associated with CRISPRi-mediated partial silencing of atpI, accC, secA and ftsZ in Pseudomonas aeruginosa PAO1. A non-targeting CRISPRi control was profiled in parallel, including an additional condition exposed to 0.4 µg/mL tobramycin. Three independent biological replicates were analyzed per condition.