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1. ⭐ GSE327132 氧气梯度影响交叉喂养，导致肠道共生菌群出现空间组织结构

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)、spatial、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : David Scheidweiler ; Elise Bornet ; Hannah Ochner ; Sonja Blascher ; Stanislas Thiriet-Rupert ; Louis Dorison ; Cristophe Beloin ; Yohan Davit ; Tanmay A. M. Bharat ; Samy Gobaa ; Alexander J. Westermann ; Kiran R. Patil ; Jean-Marc GhigoSeries Type : Expression profiling by high throughput sequencingOrganism : Bacteroides thetaiotaomicron ; Escherichia coliMicrobial interactions unfold within environments structured by physical transport, and chemical gradients, yet most mechanistic studies rely on well-mixed systems that mask the reciprocal influences of ecology and metabolism. Here, we dissected the interactions between the mammalian gut commensal Bacteroides thetaiotaomicron, a primary degrader of dietary polysaccharides, and Escherichia coli, a facultative intestinal anaerobe. In anoxic liquid culture, B. thetaiotaomicron extracellularly hydrolyzes amylopectin and releases diffusible breakdown products that E. coli assimilates, as confirmed by C¹³-starch tracing and sugar utilzation-impaired mutants. In a microfluidic system engineered to mimic intestinal crypt-like oxygen gradients, this same pair of species no longer behaves as in bulk culture, but self-organizes into complementary spatial niches. B. thetaiotaomicron colonizes anoxic regions where it degrades polysaccharides, while E. coli occupies oxygenated zones where it consumes the released sugars. Through aerobic respiration, E. coli locally reduces oxygen, widening the anoxic region that B. thetaiotaomicron subsequently invades. Disrupting sugar uptake in E. coli collapses this organization, whereas increasing oxygen availability reverses it. A reaction–transport model shows that these patterns arise from coupled feedbacks between resource release, resource consumption, and oxygen modification. Together, our results reveal how spatial structure and physicochemical gradients convert a cross-feeding interaction into a dynamic niche-construction process that stabilizes coexistence and generates emergent ecological organization.
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2. ⭐ GSE307556 整合蛋白质组学和代谢组学揭示MAT2A在非小细胞肺癌代谢重编程中的作用及其相关联合治疗策略

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolic、metabolomics、proteomics
• 📝 描述：Contributors : Yimin Chen ; Cheng Wang ; Xiongjun Wang ; Hu ZhouSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMAT2A, a key enzyme in the methionine cycle, generates S-adenosylmethionine (SAM), a critical metabolite involved in multiple metabolic pathways and epigenetic regulation. Although MAT2A is frequently overexpressed in tumors, its role in metabolic reprogramming within non-small cell lung cancer (NSCLC) remains poorly understood. Current MAT2A inhibitors, such as AG270, exhibit limited efficacy and are primarily used in MTAP-deleted tumors, highlighting the need to explore additional therapeutic strategies. Here, we employed proteomics and untargeted metabolomics in NSCLC cell lines, complemented by targeted metabolomics, RT-qPCR and ATAC-seq, to systematically characterize MAT2A-rewired metabolic reprogramming and identify potential combination treatment strategies. Totally, MAT2A knockdown or inhibition significantly disrupted fatty acid biosynthesis, cholesterol homeostasis, glycolysis and the transsulfuration pathways. In lipid metabolism, MAT2A inhibition impaired cell proliferation by suppressing fatty acid biosynthesis, and induced cholesterol biosynthesis and efflux impairment. Combining MAT2A inhibitors with the liver X receptor agonist LXR-623, which facilitated cholesterol efflux, effectively depleted intracellular cholesterol and augmented anti-tumor efficacy. In energy metabolism, MAT2A mainly inhibited glycolysis through HIF1A regulation and GLUT1 inhibitor BAY-876 demonstrated a synergetic effect when combined with AG270. In the transsulfuration pathway, MAT2A transcriptionally regulated a key enzyme CBS, and combination treatments using AG270 with either the SLC7A11 inhibitor HG106 or the PHGDH inhibitor NCT-503 exhibited enhanced anti-tumor activity. Overall, our findings identified MAT2A as a critical regulator of metabolic networks in NSCLC and propose several rational combination therapies to enhance MAT2A inhibitor efficacy.
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3. GSE342301 SIRT2 脱酰化酶调节剂控制 EBV 感染和有丝分裂激活过程中 B 细胞的代谢重编程

• ✍️ 作者：未知作者
• 🏷️ 关键词：B cell、metabolic
• 📝 描述：Contributors : Ashley P Barry ; Kaeden K Hill ; Micah A LuftigSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSirtuin-2 (SIRT2) is a cellular deacylase, regulating cell cycle progression and metabolic homeostasis. Recently, SIRT2 has emerged as a target with both anticancer and antiviral potential. However, the role and targetability of SIRT2 in viral-driven cancers remains unexplored. Epstein-Barr virus (EBV) is a ubiquitous herpesvirus with oncogenic potential that establishes latency in B lymphocytes and is typically controlled by a robust T cell immune response. In settings that compromise this response, such as immune suppression following transplant, EBV can cause B cell lymphomas. With broad immunosuppression and varying response rates limiting the effectiveness of existing lymphoma therapeutics, new strategies are necessary. SIRT2 modulation significantly alters gene expression and metabolism of EBV-infected B cells. Treatment with SIRT2 modulators drives hyperacetylation of targets involved in lipid metabolism, central carbon metabolism, and oxidative phosphorylation. EBV-positive and EBV-negative B cell lymphomas rely on glycolysis to avoid cell death after SIRT2 modulation, revealing a metabolic vulnerability that can be harnessed to kill lymphoma cells. Overall, we have identified how SIRT2 could be implicated as a novel target of therapeutic potential for B cell lymphomas, while also defining fundamental roles for extranuclear lysine acetylation in regulating B cell proliferation and metabolism.
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4. GSE330590 批量 RNA 测序揭示间皮细胞 (MC) 和癌症相关间皮细胞 (CAMC) 之间的差异基因表达

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、sequencing
• 📝 描述：Contributors : Maeva Chauvin ; David PepinSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis study presents a bulk RNA-sequencing analysis comparing mouse primary mesothelial cells (MCs) and cancer-associated mesothelial cells (CAMCs). MCs were treated for 72 hours with conditioned media derived from KPCA cancer cells or with vehicle control to induce CAMC-like reprogramming. RNA was extracted and subjected to bulk transcriptomic profiling to identify differentially expressed genes and associated biological pathways.
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5. GSE327867 SBSN在肾细胞癌进展和肿瘤血栓形成中的双重作用：通过IFI6介导的细胞自主性NF-κB-CD44激活和旁分泌血管生成

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma
• 📝 描述：Contributors : Jinming Di ; Yuedian Ye ; Jinbin Xu ; Weihao Liu ; Zhansen Huang ; Xiaoming Li ; Jiang LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensRenal cell carcinoma (RCC) is a highly vascularized malignancy with a propensity for venous invasion and tumor thrombus (TT) formation, yet the molecular mechanisms linking vascular aggression to tumor progression remain incompletely understood. In this study, we identify suprabasin (SBSN) as a key oncogenic mediator that is consistently upregulated in RCC tissues and further enriched in TT, correlating with poor patient prognosis. Functional assays demonstrate that SBSN promotes RCC cell proliferation, migration, and invasion in vitro. Transcriptomic analysis reveals activation of the NF-κB signaling pathway in SBSN-overexpressing cells, with CD44 emerging as a critical downstream effector. We further delineate a novel SBSN-NF-κB-CD44 axis that drives malignant phenotypes in RCC cells. In vivo, SBSN knockdown attenuates tumor growth and induces a shift in epithelial-mesenchymal transition (EMT) markers. Clinically, SBSN expression in RCC tissue positively correlates with microvessel density (MVD). Mechanistically, tumor-secreted SBSN enhances angiogenesis through a paracrine pathway by upregulating the anti-apoptotic protein IFI6 in endothelial cells, thereby suppressing cleaved caspase-3 and Bax activation and promoting endothelial survival and tube formation. Collectively, our findings uncover a dual role for SBSN in RCC progression: intrinsically via the NF-κB-CD44 axis to drive tumor cell aggressiveness, and extrinsically via the SBSN-IFI6 axis to promote angiogenesis and TT formation. This study positions SBSN as a potential prognostic biomarker and therapeutic target to disrupt both tumor growth and vascular support in advanced RCC.
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6. GSE308983 重编程谱系特征促进癌细胞的上皮行为 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、ChIP-seq
• 📝 描述：Contributor : Lance TeradaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCancer cells distort epigenetic control of gene expression, allowing for a remarkable degree of plasticity and loss of cell type identity. At the same time, expression of identity-discordant lineage determinants can significantly shift cell phenotype by creating lineage hybrid states. One example is the misexpression of IKZF3, encoding the lymphocyte restricted transcription factor Aiolos, by roughly half of non-small cell lung carcinomas (NSCLC) and the majority of small cell lung carcinomas [1]. During normal lymphocyte development, pre-B progenitors enter a proliferative phase dependent on survival cues from bone marrow stroma. To progress, Aiolos and its paralog Ikaros (IKZF1) repress multiple adhesion-related genes, releasing cells from this epithelial-type dependence on solid matrix in preparation for their release as mature lymphocytes into the circulation [2, 3]. In lung cancers, unlicensed expression of Aiolos initiates a similar shift from an epithelial to a lymphocyte-like state by repression of multiple adhesion-related genes, resulting in loss of anoikis and consequent metastatic spread [1]. To reverse these lymphoid traits, we created a chimeric epigenetic editor designed to specifically retrieve Aiolos-repressed epithelial adhesion properties. Here, we demonstrate proof of principle for epithelial lineage restoration by exploiting a lymphocyte developmental pathway.
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7. GSE308846 重编程谱系特征促进癌细胞的上皮行为 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、ATAC-seq
• 📝 描述：Contributor : Terada LanceSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCancer cells distort epigenetic control of gene expression, allowing for a remarkable degree of plasticity and loss of cell type identity. At the same time, expression of identity-discordant lineage determinants can significantly shift cell phenotype by creating lineage hybrid states. One example is the misexpression of IKZF3, encoding the lymphocyte restricted transcription factor Aiolos, by roughly half of non-small cell lung carcinomas (NSCLC) and the majority of small cell lung carcinomas [1]. During normal lymphocyte development, pre-B progenitors enter a proliferative phase dependent on survival cues from bone marrow stroma. To progress, Aiolos and its paralog Ikaros (IKZF1) repress multiple adhesion-related genes, releasing cells from this epithelial-type dependence on solid matrix in preparation for their release as mature lymphocytes into the circulation [2, 3]. In lung cancers, unlicensed expression of Aiolos initiates a similar shift from an epithelial to a lymphocyte-like state by repression of multiple adhesion-related genes, resulting in loss of anoikis and consequent metastatic spread [1]. To reverse these lymphoid traits, we created a chimeric epigenetic editor designed to specifically retrieve Aiolos-repressed epithelial adhesion properties. Here, we demonstrate proof of principle for epithelial lineage restoration by exploiting a lymphocyte developmental pathway.
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8. GSE324006 MEF2C 控制与巨噬细胞中阿尔茨海默病风险相关的溶酶体和脂质清除程序 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、scRNA
• 📝 描述：Contributors : Anna Podlesny-Drabiniok ; Edoardo Marcora ; Alison Goate ; Tulsi PatelSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensRisk alleles for late-onset Alzheimer’s disease (AD) are enriched in myeloid cis-regulatory elements, implicating myeloid gene-regulatory networks in disease susceptibility. A conserved lipid-associated transcriptional signature—spanning disease-associated microglia and peripheral lipid-associated macrophages (DLAM)—emerges across neurodegenerative and metabolic diseases, yet the transcriptional regulators of this gene expression program remain incompletely defined. Here, we show that MEF2C—a candidate AD risk gene—is a master DLAM regulator. Using MEF2C knockout and knockdown in human iPSC-derived microglia and macrophages, we found that total or partial MEF2C loss is sufficient to induce DLAM-associated transcriptional, epigenomic, and functional remodeling, including enhanced lysosomal activity and cholesterol efflux. Integration of chromatin accessibility and regulatory epigenetic profiles with functionally informed fine-mapping linked AD causal variants in other loci to MEF2C-regulated regulatory regions and downstream risk genes. In a triculture model of AD, microglial MEF2C loss is associated with an increased DLAM population and a reduced Aβ42/40 ratio, supporting context-dependent reprogramming of microglia as a mechanism to modulate AD-relevant pathology.
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9. GSE323981 MEF2C 控制与巨噬细胞中阿尔茨海默病风险相关的溶酶体和脂质清除程序 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、ATAC-seq
• 📝 描述：Contributors : Anna Podlesny-Drabiniok ; Edoardo Marcora ; Alison Goate ; Tulsi PatelSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensRisk alleles for late-onset Alzheimer’s disease (AD) are enriched in myeloid cis-regulatory elements, implicating myeloid gene-regulatory networks in disease susceptibility. A conserved lipid-associated transcriptional signature—spanning disease-associated microglia and peripheral lipid-associated macrophages (DLAM)—emerges across neurodegenerative and metabolic diseases, yet the transcriptional regulators of this gene expression program remain incompletely defined. Here, we show that MEF2C—a candidate AD risk gene—is a master DLAM regulator. Using MEF2C knockout and knockdown in human iPSC-derived microglia and macrophages, we found that total or partial MEF2C loss is sufficient to induce DLAM-associated transcriptional, epigenomic, and functional remodeling, including enhanced lysosomal activity and cholesterol efflux. Integration of chromatin accessibility and regulatory epigenetic profiles with functionally informed fine-mapping linked AD causal variants in other loci to MEF2C-regulated regulatory regions and downstream risk genes. In a triculture model of AD, microglial MEF2C loss is associated with an increased DLAM population and a reduced Aβ42/40 ratio, supporting context-dependent reprogramming of microglia as a mechanism to modulate AD-relevant pathology.
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10. GSE304995 HIV-1 通过损害抗原特异性与树突状细胞的通讯来重编程 CD4 T 细胞反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、antigen
• 📝 描述：Contributor : Katharina MorathSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHIV-1 infection causes general dysfunction of adaptive immune cells that persists even under therapy but the underlaying mechanisms remain elusive. Antigen-specific interactions of the main target cells of HIV, CD4 T cells, with dendritic cells (DCs) orchestrate global T cell responses and convey help to CD8 T cells. Here we report that HIV-1, by virtue of its pathogenesis factor Nef, impairs activation and transcriptionally reprograms CD4 T cells to dampen Th1 differentiation in response to antigen-specific stimulation by DCs. These alterations also disrupt functional communication to DCs to reduce DC activation and limit Th1 helper cytokine production. Mechanistically, Nef achieves this modulation of antigen-specific CD4 T cell function by reducing T cell surface levels of CD4. These results define modulation of CD4 T cell-DC communication as pathogenic principle by which HIV-1 disrupts adaptive immunity and emphasize the direct role of CD4 in immune cell communication.
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1. 介绍 Bioconductor 学生-ECR 委员会

• ✍️ 作者：未知作者
• 🏷️ 关键词：Bioconductor
• 📝 描述：Announcing the Bioconductor Student-ECR Council From an idea that hatched during the EuroBioC2026 Birds of a Feather session, we are super excited to announce the formation of the Student-ECR Council! As a newly established Council, we aim… Continue reading: Introducing the Bioconductor Student-ECR Council
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• GSE272424 通过靶向肿瘤相关巨噬细胞的嵌合受体工程溶瘤病毒恢复内源性抗肿瘤免疫力
• GSE342712 Claudin 5 通过调节脑微血管内皮细胞的增殖、迁移和粘附来调控血脑屏障通透性，从而预防肺癌转移
• GSE336257 长读 RNA 测序揭示了接受放射治疗的健康小胶质细胞系中的异构体转换模式。
• GSE334227 MDM2 结合并抑制 RNA 聚合酶 III，从而抑制针对胞质 DNA 的先天免疫反应
• GSE328705 肾细胞癌中肿瘤内Vd2+ γdT细胞的细胞毒性和炎症功能差异
• GSE318672 患有 BPD 的婴儿具有以波形蛋白表达和纤毛丢失为特征的气道内型 [RNA-seq P199-6]
• GSE318577 患有 BPD 的婴儿具有以波形蛋白表达和纤毛丢失为特征的气道内型 [RNA-Seq P199-8]
• GSE318575 患有 BPD 的婴儿具有以波形蛋白表达和纤毛丢失为特征的气道内型 [RNA-Seq P199-7]
• GSE318546 患有 BPD 的婴儿具有以波形蛋白表达和纤毛丢失为特征的气道内型 [RNA-seq P199-4Data]
• GSE318544 患有 BPD 的婴儿具有以波形蛋白表达和纤毛丢失为特征的气道内型 [RNA-Seq P199-9Data]
• GSE313406 母体暴露于空气污染会改变青春期前后后代对臭氧的产后代谢反应。
• GSE308182 重编程谱系特征促进癌细胞的上皮行为
• GSE306607 HeLa细胞RNA测序，包含随机序列对照和CNOT11敲低
• GSE306116 Caspase-3 控制帕金森病期间小胶质细胞中的 RNA 剪接和线粒体动力学 [RNA-Seq]
• GSE294641 SPLEVs，一种治疗细胞因子风暴综合征的新疗法
• GSE249970 对用 EVs 或 SPLEVs 治疗的 LPS 诱导 ARDS 模型小鼠肺组织进行转录组分析。
• GSE225153 碳环 5-氮杂-2’-脱氧胞苷抗代谢物增加 TET 表达和 5-羟甲基胞嘧啶形成 [RNA-seq]
• GSE225152 碳环 5-氮杂-2’-脱氧胞苷抗代谢物 [甲基化] 增加 TET 表达和 5-羟甲基胞嘧啶形成
• GSE323984 MEF2C 控制与巨噬细胞中阿尔茨海默病风险相关的溶酶体和脂质清除程序 [bulkRNAseq_WTC11_iMGL]
• GSE323982 MEF2C 控制与巨噬细胞中阿尔茨海默病风险相关的溶酶体和脂质清除程序 [scRNAseq_WTC11_iMGL_ReN]
• GSE319124 下一代儿科癌症模型：患者匹配的原位异种移植、3D 类器官、2D 培养和细胞系用于识别儿科实体瘤的治疗弱点 [scRNAseq]
• GSE307254 系统性发现转录变异的潜在调控因子揭示 NAP1L1 是小鼠 ESC 中的转录稳定剂 [scRNA-seq]
• GSE342610 利用培养的胶质母细胞瘤模型进行甲基化芯片分析，以构建替代性拷贝数变异（CNV）谱。
• GSE342137 C57BL6 和 NOD 小鼠品系 NK 细胞转录组的比较
• GSE334311 CCR10 调节的粘膜免疫反应支持 SARS-CoV-2 感染后肺组织稳态的恢复。
• GSE328496 SAHA 治疗后三体海马神经元的基因表达 + ATAC 分析 [RNA-seq]
• GSE328495 SAHA 治疗后三体海马神经元的基因表达 + ATAC 分析 [ATAC-seq]
• GSE303314 UVB 诱导的 BRAFV600E 小鼠黑色素瘤肿瘤（有或无 p38α）的转录谱（整个肿瘤、CD45⁺ 和 CD45⁻ 群体）
• GSE281001 C3-C3aR轴调节肺泡巨噬细胞的训练免疫
• GSE342640 胰岛素抵抗与人类泌乳初期乳腺线粒体功能障碍相关
• GSE294426 长期活体成像揭示小鼠表皮干细胞层级的性别二态性 [scRNA-Seq]