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。

• Ribosome profiling of OTUD6B knockdown and scramble-control MDA-MB-231 cells
  GSE352635Homo 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
• Effects of orexin-A on human dermal papilla cells
  GSE352146Homo sapiens6 个样本2026-10-30

  We examined effects of orexin-A on human dermal papilla cells.
• StrataChip: a microphysiological system to capture dynamic keratinocyte fate and mechanical transitions during human epidermal morphogenesis
  GSE351999Homo 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
• Transcriptomic profiling of human nucleus pulposus cells following Mulberrin treatment
  GSE351312Homo 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.
• GPS2 attenuates cigarette smoke-induced airway epithelial injury by attenuating mitochondrial oxidative stress
  GSE347944Homo 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.
• RNA-bound MYBL2 engages the oncogenic transcription factors MAFG and FRA1 to promote melanoma
  GSE335104Homo sapiens9 个样本2026-10-30

  Non-mutational mechanisms, including copy number alterations and transcription factor dysregulation, are critical drivers of melanoma progression. We identify the transcription factor MYBL2 as a key oncogenic driver located on frequently amplified chromosome 20q. MYBL2 overexpression promotes transformation and correlates with poor survival, yet paradoxically, its transactivation function is dispensable for oncogenic activity. Instead, MYBL2 acquires a previously unrecognized non-canonical RNA binding function in melanoma cells enabled by the melanoma-associated RNA landscape. Through these RNA interactions, MYBL2 reshapes the chromatin landscape toward an AP-1 permissive state and promotes chromatin association of the oncogenic transcription factors MAFG and FRA1, indirectly reprogramming tumor-promoting gene networks whose expression predicts poor outcomes across multiple cancers. Importantly, disrupting the MYBL2-RNA interaction using a small decoy RNA impairs MYBL2 association with MAFG and FRA1 and suppresses melanoma cell growth. Our findings establish MYBL2 as an RNA binding-dependent, 20q gain-associated driver of melanoma and reveal that MYBL2-RNA interactions promote melanoma progression through chromatin and transcriptional network remodeling.
• Detection of a sequence feature for recursive splicing
  GSE327295Homo sapiens5 个样本2026-10-30

  RNA splicing is directed by cis-acting sequence signals interacting with trans-acting factors to remove introns from newly transcribed pre-mRNA, joining exons to generate mature mRNA. Splicing happens far more often than observed exon-exon junctions in mRNA. As one contributing process, the spliceosome progressively removes large introns in small segments by ‘recursive splicing’, instead of splicing the whole intron at one time. However, the cis-acting sequences associated with recursive splicing have not been identified. Using probabilistic mixture models, we found that recursive splicing occurs more frequently in first introns, which are typically longer, and exhibit a distinct CG-rich sequence feature in the sequences flanking the upstream 5’SS, and depletion of CGs in the downstream polypyrimidine tract. Remarkably, recursive splicing is also more frequent in downstream introns of genes containing first introns with these properties. Mechanistically, these data suggest that early events in RNA synthesis and processing influence the prevalence of recursive splicing for the rest of the transcript. Finally, we developed a sequence-dependent classifier for recursive splicing, which we tested with a novel medium-throughput primer extension assay. In summary, the usage of recursive splicing sites is established at the beginning of RNA synthesis through newly-identified sequence motifs flanking both ends of the first intron.

  计算与 AI
• Aberrant stabilization of the m6A reader IGF2BP3 drives metastatic progression and 5-FU refractoriness in FBXW7-mutant colorectal cancer
  GSE326794Homo sapiens4 个样本2026-10-30

  Loss of the E3 ubiquitin ligase FBXW7 leads to aberrant stabilization of the m6A reader IGF2BP3 in colorectal cancer. To identify the RNA targets of IGF2BP3 under FBXW7-deficient conditions, we performed HITS-CLIP-seq in isogenic DLD1 FBXW7 wild-type and knockout cell lines. CLIP-seq analysis revealed that IGF2BP3-binding sites were enriched in 3' UTR regions of protein-coding mRNAs, and that IGF2BP3 preferentially bound cancer-promoting transcripts including DPYD and COL4A1.
• Establishment of a multi-stage in vitro screening platform to identify candidate compounds for intestinal mucosal damage in inflammatory bowel disease
  GSE321659Homo sapiens9 个样本2026-10-30

  Mucosal healing is a key therapeutic goal in inflammatory bowel disease (IBD), which is characterized by mucosal lesions in the gastrointestinal tract. For IBD drug development, it is important to identify multiple compounds with strong effects on mucosal injury and different mechanisms of action. Here, we established an intestinal organoid-based assay to evaluate cytokine-induced inflammatory and epithelial stress responses. We also developed an intestinal microphysiological system (intestinal MPS)-based assay for quantitative evaluation of cytokine-induced changes in mucosal architecture. By integrating these assays, we constructed a multi-stage screening platform to identify candidate compounds that suppress inflammatory responses and preserve mucosal architecture. Tofacitinib, an approved IBD drug, showed positive effects in these assays, supporting the relevance of this platform. Although organoid-based screening identified pimitespib as a candidate compound, pimitespib did not improve mucosal architecture in the intestinal MPS. Consistently, pimitespib failed to restore mucosal morphology in an IBD mouse model. These findings suggest that combining intestinal organoids with an intestinal MPS may help identify candidate compounds that suppress inflammatory responses while preserving mucosal architecture.
• A Cross-scale Causal Mapping Framework Pinpoints Macrophage Orchestrators of Balanced Arterial Development
  GSE317047Homo sapiens3 个样本2026-10-30

  This dataset contains single-cell RNA sequencing profiles of induced pluripotent stem cell (iPSC)-derived blood vessel organoids (BVOs) cultured under different macrophage co-culture conditions. The aim is to investigate the regulation of vascular maturation and arterial development by the immune system. The BVOs were cultured either alone or with two polarized populations of iPSC-derived macrophages: activated (MGL low) and regenerative (MGL high). Single-cell transcriptomic analyses revealed polarization-dependent transcriptional changes in vascular endothelial and perivascular cell populations. This dataset allows for the identification of candidate genes and signaling pathways associated with arterial specification, vessel stabilization, and vascular maturation in a human organoid model.

  单细胞
• HOXA9 Couples Transcriptional Control with Higher-Order Chromatin Architecture in Acute Myeloid Leukemia [HiC]
  GSE306376Homo sapiens6 个样本2026-10-30

  The three-dimensional (3D) genome is organized by architectural proteins such as CTCF and cohesin, while transcription factors (TFs) typically regulate enhancer–promoter (E–P) and enhancer-enhancer (E-E) communications without major structural effects. How these layers intersect remains unclear. Here, we reveal that the homeobox TF HOXA9—overexpressed in ~50% of acute myeloid leukemia (AML)—exerts a non-canonical architectural role. HOXA9 depletion in AML cells disrupts topologically associating domain (TAD) boundaries, dissolves chromatin loops, and perturbs cell-specific gene programs. We identify a distinct class of long-range “hybrid” loops (>250 kb) co-anchored by HOXA9 and convergent CTCF, frequently linked to TAD boundaries. Integrative analysis defines a 3D genome informed HOXA9 network and identifies NHLRC2 as a direct downstream target essential for leukemogenesis. Our findings establish HOXA9 as a dual-function TF that couples transcriptional control with higher-order genome architecture, offering a new mechanism for its pervasive activation across molecularly diverse AML subtypes.

  扰动筛选
• Multi-lineage evolution of drug resistance via a keratin 17+ aberrant basaloid drug tolerant persister population in EGFR-mutant NSCLC
  GSE303284Homo sapiens6 个样本2026-10-30

  We have an incomplete understanding of how EGFR-mutant drug tolerant persister cells (DTPCs) adapt to tolerate EGFR signaling blockade and whether these different mechanisms of resistance are present at baseline or emerge from a common DTPC population. In this study, we leveraged single cell RNA sequencing to comprehensively characterize phenotypes potentiating EGFR-mutant DTPCs and minimal residual disease states in part by sampling in vitro model systems. Using this and other single cell RNA sequencing data, we uncovered that a recurrent, novel KRT17+/KRT5- DTPC population harboring basaloid features and decreased alveolar lineage fidelity could give rise to diverse, multilineage mechanisms of targeted therapy resistance.

  单细胞
• HOXA9 Couples Transcriptional Control with Higher-Order Chromatin Architecture in Acute Myeloid Leukemia [RNA-seq]
  GSE301086Homo sapiens8 个样本2026-10-30

  The three-dimensional (3D) genome is organized by architectural proteins such as CTCF and cohesin, while transcription factors (TFs) typically regulate enhancer–promoter (E–P) and enhancer-enhancer (E-E) communications without major structural effects. How these layers intersect remains unclear. Here, we reveal that the homeobox TF HOXA9—overexpressed in ~50% of acute myeloid leukemia (AML)—exerts a non-canonical architectural role. HOXA9 depletion in AML cells disrupts topologically associating domain (TAD) boundaries, dissolves chromatin loops, and perturbs cell-specific gene programs. We identify a distinct class of long-range “hybrid” loops (>250 kb) co-anchored by HOXA9 and convergent CTCF, frequently linked to TAD boundaries. Integrative analysis defines a 3D genome informed HOXA9 network and identifies NHLRC2 as a direct downstream target essential for leukemogenesis. Our findings establish HOXA9 as a dual-function TF that couples transcriptional control with higher-order genome architecture, offering a new mechanism for its pervasive activation across molecularly diverse AML subtypes.

  扰动筛选
• Heightened DOT1L-AF10 enriches H3K79me3 to promote pro-atherogenic inflammatory endothelial phenotype through NF-κB p65
  GSE295366Homo sapiens3 个样本2026-10-30

  DOT1L-catalyzed H3K79 methylation is a hallmark of actively transcribed genes and has been extensively studied in developmental and disease contexts. While DOT1L inhibition has emerged as a promising therapeutic strategy in cancer, its role in pro-atherogenic endothelial inflammation remains unclear. To investigate this, we utilized an in vivo partial carotid artery ligation model and observed increased DOT1L expression and H3K79me3 level. Consistently, in vitro studies employing a 3D-printed human coronary artery model and TNF-α stimulation corroborated these results, showing elevated DOT1L expression and H3K79me3 deposition, while levels of H3K79me and me2 remained unchanged. Further analyses identified key DotCom complex components, AF10 and AF9 (upregulated) and AF17 (downregulated), as contributors to the enhanced H3K79me3 landscape. CUT&RUN sequencing showed prominent H3K79me3 enrichment at the RELA (NF-κB p65) promoter, corresponding with increased NF-κB p65 expression and activation. Notably, inhibition/knockdown of the methyltransferase DOT1L or overexpression of the demethylase FBXL10 significantly reduced H3K79me3 levels, thereby suppressing NF-κB p65 expression and attenuating endothelial inflammation, independent of canonical NF-κB p65 activation. These findings establish DOT1L-mediated H3K79me3 as a crucial epigenetic regulator of endothelial inflammation, highlighting a potential therapeutic avenue for mitigating NF-κB p65-driven pro-atherogenic endothelial dysfunction.
• AR-V7 condensates drive androgen-independent transcription in castration resistant prostate cancer
  GSE292445Homo sapiens6 个样本2026-10-30

  Biomolecular condensates organize cellular environments and regulate key processes like transcription. We previously showed that full-length androgen receptor (AR-FL), a major oncogenic driver in prostate cancer (PCa), forms nuclear condensates upon androgen stimulation in androgen-sensitive PCa cells. Disrupting these condensates impairs AR-FL transcriptional activity, highlighting their importance. However, resistance to androgen deprivation therapy often leads to castration-resistant prostate cancer (CRPC), driven by constitutively active splice variants like AR variant 7 (AR-V7). The mechanisms underlying AR-V7’s role in CRPC remain unclear. We characterized AR-V7’s condensate-forming ability and compared its phase behavior with AR- FL across PCa models and in vitro. Our findings indicate that cellular context influences AR-V7’s condensate formation. Unlike AR-FL, AR-V7 spontaneously forms condensates without androgen stimulation and functions independently of AR-FL in CRPC. However, AR-V7 requires a higher concentration to form condensates in cells and in vitro. We reveal that AR-V7 drives transcription through condensate-dependent and independent mechanisms. Using an AR-V7 mutant incapable of forming condensates but retaining nuclear localization and DNA binding, we show the condensate-dependent regime activates part of the oncogenic KRAS pathway in CRPC. Genes under this regime harbored more AR-binding sites and exhibited boosted expression in response to AR-V7. These findings uncover AR-V7 condensates’ role in oncogenic transcription and CRPC progression.
• Species-Dependent WNT/ß-Catenin Signaling Orchestrates Epiblast Morphogenesis during Early Implantation [Cut & Run]
  GSE273593Homo sapiens4 个样本2026-10-30

  The precise orchestration of epiblast tissue remodeling during implantation is critical for mammalian embryonic development and the regulatory link between cellular signaling and epiblast tissue morphogenesis remains unexplored. We present a fully defined, 3D epiblast-like model derived from human pluripotent stem cells (hPSCs). Functional studies of these in vitro models, alongside in vivo investigations in human and mouse embryos, reveal the pivotal role of canonical WNT signaling in mammalian epiblast morphogenesis. In humans, WNT/β-catenin signaling is crucial for epithelization, rosette formation, and cavitation of epiblast tissue. In mice, inhibition of canonical WNT signaling supports these events. Dual CUT&RUN and RNA sequencing, complemented by multi-study comparative transcriptome profiling, identify a TCF/LEF-mediated mechanism linking WNT signaling to lipid metabolism in human epiblast morphogenesis. This study highlights divergent roles of WNT-mediated mechanisms in early mouse and human development, as well as potential causes of human embryo lethality at implantation.
• Identification of 2’-O-methylation sites on mRNA and pre-mRNA
  GSE188194Homo sapiens6 个样本2026-10-30

  There have been reports suggesting that there may be thousands of Nm-modified mRNA or pre-mRNA transcripts in mammalian cells, there have been no studies that validate the proposed sites or determine the molecular mechanism responsible for their placement. In this study, we have refined a method for transcriptome-wide mapping of Nm sites and identified numerous high-confidence sites in mature mRNA
• BAP1 safeguards double-strand DNA break repair by limiting DNA end resection [ChIP-Seq]
  GSE352106Homo sapiens5 个样本2026-10-29

  The tumor suppressor BAP1 is frequently mutated in uveal melanoma and has been linked to homologous recombination (HR), yet how it influences DNA double-strand break (DSB) repair pathway choice remains unclear. Here, we identify BAP1 as a critical regulator that restricts DNA end resection to preserve non-homologous end-joining (NHEJ) capacity. Loss of BAP1 leads to aberrant accumulation of H2AK119 ubiquitination at DSBs, driving unscheduled resection in G1-phase cells and impairing recruitment of the anti-resection factor 53BP1. Co-depletion of the resection initiator CtIP restores NHEJ efficiency in BAP1-depleted cells, and pharmacological suppression of H2AK119 ubiquitination reverses these defects, placing unscheduled resection causally upstream of the end-joining failure. RNA sequencing and genome-wide H2AK119ub profiling show that neither the expression of NHEJ and HR genes nor the H2AK119ub landscape at their promoters is appreciably altered by BAP1 loss, supporting a role of altered H2AK119ub at the DSBs. These findings indicate that BAP1 safeguards DSB repair fidelity by preventing hyper-resection, thereby maintaining NHEJ competence. Consistent with this role, BAP1-depleted cells accumulate micronuclei, and BAP1 loss is associated with genomic instability in human uveal melanoma. Together, our results uncover a mechanism by which chromatin regulation constrains resection to coordinate repair pathway utilization.
• Transcriptional response of primary human pancreatic cancer-associated fibroblasts to IFN-γ and lipopolysaccharide stimulation
  GSE348821Homo sapiens9 个样本2026-10-29

  Single-cell analysis of a pan-cancer tumor microenvironment atlas identified transcriptionally distinct inflammatory cancer-associated fibroblast (iCAF) subpopulations, including an ISG15+ iCAF population predicted to arise downstream of interferon-γ signaling from CD8+/GZMB+ T cells, and a CXCL8+ iCAF population. To test these predictions experimentally, primary cancer-associated fibroblasts (CAFs) were isolated from a fresh human pancreatic ductal adenocarcinoma (PDAC) surgical specimen, expanded in culture, and treated for 24 hours with control media, recombinant human interferon-γ, or lipopolysaccharide (LPS). Bulk RNA-sequencing of the resulting nine libraries was used to compare the induced transcriptional programs against gene signatures derived from the ISG15+ iCAF and CXCL8+ iCAF subpopulations of the atlas. Results are reported in the associated publication.

  单细胞细胞图谱
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [scATAC-seq]
  GSE326466Homo sapiens3 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation. Here we performed snATAC-seq to gain further insight into the open accessible chromatin regions in various insulinoma cell types.

  单细胞
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [Multiome]
  GSE326458Homo sapiens2 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation. Here we performed multiome assay to delineate open accessible chromatin regions and single cell transcriptomic profiles in various insulinoma cell types.

  单细胞多组学
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [snRNA-seq]
  GSE326455Homo sapiens2 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation in insulinomas. Here we performed snRNAseq to gain further insight into the transcriptomic profiles of various insulinoma cell types.

  单细胞
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [ChIP-seq]
  GSE326450Homo sapiens7 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation in insulinomas. Here we performed bulk RNA-seq to gain further insight into the transriptomic profiles of insulinomas and FACS-sorted beta cells.
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [ATAC-seq]
  GSE326447Homo sapiens7 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation in insulinomas. Here we performed bulk ATAC-seq to gain further insight into the open accessible chromatin regions in insulinomas and FACS-sorted beta cells.
• A CRISPR-Based Humanized Model Reveals Cooperative Role of STAG2 Loss in Familial GATA2-Deficient MDS Progression
  GSE317264Homo sapiens6 个样本2026-10-29

  Myelodysplastic syndrome is a heterogeneous myeloid malignancy driven by hematopoietic stem cell dysfunction, leading to ineffective hematopoiesis and cytopenias. Familial GATA2 deficiency is the most common cause of Myelodysplastic syndrome in adolescents, with progression often accelerated by co-occurring mutations, notably STAG2 loss-of-function. Using CRISPR/Cas9-mediated genome engineering in primary human fetal liver-derived hematopoietic stem cells and xenotransplantation in mice, we modeled GATA2-deficient Myelodysplastic syndrome with acquired STAG2 loss to investigate disease initiation and progression. While GATA2 deficiency alone had minimal short-term impact in our model, combined GATA2 and STAG2 loss increased hematopoietic stem cell maintenance and self-renewal, induced a myeloid-lineage bias, and expanded primitive progenitors. Single-cell transcriptional profiling revealed upregulation of stemness genes and inflammatory pathways, alongside downregulation of MYC targets. This humanized model faithfully recapitulates high-risk GATA2-deficient Myelodysplastic syndrome, providing mechanistic insight into how cooperative mutations drive stem cell expansion, inflammatory signaling, and myeloid skewing.

  单细胞
• Non-canonical RNA binding of the MYBL2 transcription factor promotes melanoma (CLIP-seq)
  GSE284545Homo sapiens3 个样本2026-10-29

  Melanoma originates from melanocytes, and the process of melanocyte malignant transformation is affected by various factors, including non-mutational gene alterations. MYBL2 is a transcription factor primarily known for its role in regulating cell cycle progression. In this study, we characterized that MYBL2 gain or amplification occurs in one fifth of the melanoma patients, and the aberrantly upregulated MYBL2 promotes melanoma growth while representing a melanoma vulnerability. Notably, MYBL2 can also binds RNA, and its oncogenic effect is mediated through its RNA binding function. Crosslinking-immunoprecipitation followed by high-throughput sequencing revealed that MYBL2 primarily binds protein-coding genes and introns. Interestingly, MYBL2 does not affect the RNA metabolism of its direct targets. Instead, its RNA binding function influences its association with chromatin and thereby rewiring the transcription program favoring poor patient survival. Surprisingly, we observed that MYBL2 binds RNA exclusively in melanoma cells, but not in melanocytes. This phenomenon is primarily due to the altered RNA background developed following melanoma transformation, while alternations within MYBL2 itself also involved in a lesser extent. Therefore, our work identified a novel oncogenic function of MYBL2 through its RNA binding activity, extending our current understanding of MYBL2 and highlighting a critical mechanism in melanoma progression.
• Transcriptomic profiling of ECV304 cells under normoxic, hypoxic, and hypoxia-tolerant conditions
  GSE352293Homo sapiens9 个样本2026-10-28

  This study investigated transcriptomic changes in ECV304 cells under normoxic, hypoxic, and hypoxia-tolerant conditions. Cells were assigned to three groups, each with three biological replicates. The hypoxia group was exposed to 3% O2 for 24 h, whereas hypoxia tolerance was established by repeated hypoxia-reoxygenation cycles (cycle details to be confirmed). Total RNA was subjected to paired-end RNA sequencing on an Illumina NovaSeq 6000. The dataset supports comparisons of gene expression patterns associated with acute hypoxia and hypoxia tolerance.
• Super-enhancer NR125945 drives prostate cancer malignancy via long-range chromatin interactions [CUT&Tag]
  GSE346319Homo sapiens3 个样本2026-10-28

  Genetic susceptibility plays an essential role in prostate cancer (PCa) risk, while the functional mechanisms underlying several classic risk loci remain largely uncharacterized. Here, we identified a PCa specific super-enhancer within 1q42.3 locus, termed NR125945-SE. Through comparative H3K27ac ChIP-seq analysis, we observed that NR125945-SE is highly active in PCa cells compared to normal controls. NR125945-SE contributes to PCa malignant progression. Mechanistically, integrative analysis combining RNA-seq and 4C-seq data revealed that NR125945-SE regulates the expression of CAPN2 and KRT19 through long-range chromatin interactions. Furthermore, we demonstrated that NR125945-SE activity is mediated by the cooperative binding of multiple transcription factors. In summary, our findings provide insights into a functional epigenetic element within a classic genetic risk locus, proposing a mechanism by which super-enhancer-mediated regulation promotes prostate cancer progression.
• Super-enhancer NR125945 drives prostate cancer malignancy via long-range chromatin interactions [4C-Seq]
  GSE346318Homo sapiens3 个样本2026-10-28

  Genetic susceptibility plays an essential role in prostate cancer (PCa) risk, while the functional mechanisms underlying several classic risk loci remain largely uncharacterized. Here, we identified a PCa specific super-enhancer within 1q42.3 locus, termed NR125945-SE. Through comparative H3K27ac ChIP-seq analysis, we observed that NR125945-SE is highly active in PCa cells compared to normal controls. NR125945-SE contributes to PCa malignant progression. Mechanistically, integrative analysis combining RNA-seq and 4C-seq data revealed that NR125945-SE regulates the expression of CAPN2 and KRT19 through long-range chromatin interactions. Furthermore, we demonstrated that NR125945-SE activity is mediated by the cooperative binding of multiple transcription factors. In summary, our findings provide insights into a functional epigenetic element within a classic genetic risk locus, proposing a mechanism by which super-enhancer-mediated regulation promotes prostate cancer progression.
• Hypoxia-Driven CA2 Promotes Trophoblast Dysfunction in Preeclampsia
  GSE342874Homo sapiens6 个样本2026-10-28

  Objective: Explore the potential function of Carbonic Anhydrase 2 (CA2) in the pathophysiology of preeclampsia. Methods: Peripheral blood and placental samples were collected from healthy pregnant women and patients with preeclampsia. Placental CA2 expression was validated in independent clinical cohorts and experimental mouse models. HTR-8/SVneo cells was cultured and transfected with a CA2 overexpression plasmid to evaluate trophoblast dysfunction. Bulk RNA sequencing was performed to identify downstream genes associated with CA2 overexpression, followed by VEGFA rescue experiments. Hypoxia-related regulation of CA2 was investigated. Lipid nanoparticle (LNP)-encapsulated siRNA against CA2 was constructed in an L-NAME-induced PE model to evaluate therapeutic effects. Results: CA2 expression was significantly increased in placental tissues and maternal serum from women with PE and was also elevated in experimental PE mouse models.CA2 predominantly localized in trophoblast cells, and correlated positively with serum creatinine and urea and correlated negatively with fetal birth weight. CA2 overexpression markedly suppressed trophoblast proliferation, migration, and invasion, without affecting apoptosis. Transcriptomic analysis suggested that vascular endothelial growth factor A (VEGFA) acted as a downstream mediator of CA2, and VEGFA overexpression partially rescued CA2-induced trophoblast dysfunction. CA2 expression was upregulated under hypoxic conditions and regulated by hypoxia-inducible factor-1α (HIF-1α). LNP-mediated CA2 silencing partially improved placental structure and fetal outcomes in vivo. Conclusion: CA2 is upregulated in the preeclamptic placenta and is associated with placental dysfunction and adverse fetal outcomes. Mechanistically, CA2 may act downstream of HIF-1α and contribute to trophoblast dysfunction partly through modulation of VEGFA signaling, and CA2 silencing partially improved maternal and fetal outcomes, highlighting CA2 as a potential therapeutic target for preeclampsia.