详细内容（前10条）

1. ⭐ GSE335452 单细胞 RNA 测序和空间转录组学表征胰腺导管腺癌中的 CD8+ 耗竭 T 细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Jing Mao ; Chenxin Yan ; Ying Mei ; Yanjun Yao ; Xingxia Yang ; Jing Zhuang ; Kuai Yu ; Gangzhao Gu ; Hengzhi Zhang ; Yu Zheng ; Yunyao Wei ; Shuwen Han ; Qiang YanSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensPancreatic cancer resists immunotherapy due to a suppressive immune microenvironment where CD8⁺ T cells play a key role. Using single‑cell RNA sequencing and spatial transcriptomics, we characterized CD8⁺ exhausted T (Tex) cells in pancreatic ductal adenocarcinoma (PDAC). We generated single‑cell profiles from PDAC tumors and matched peripheral blood mononuclear cells, and performed T cell sub‑analysis. We found CXCL13 upregulated and GZMK downregulated in CD8⁺ Tex cells. Cell‑cell interaction analysis showed that T cells most frequently interacted with myeloid cells and cancer cells via ligand‑receptor pairs; INHBA⁺ macrophages and cancer cells communicated most with CD8⁺ Tex cells. Two key LR pairs (SPP1–integrin α4β1 and PLAUR–integrin α4β1) mediated crosstalk between cancer cells and CD8⁺ Tex cells, confirmed by immunofluorescence, spatial mapping, and protein docking. High SPP1 and PLAUR expression correlated with poor prognosis in TCGA‑PAAD. These findings provide a resource for understanding CD8⁺ T cell exhaustion in PDAC.
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2. ⭐ GSE315797 肿瘤特异性RNA编辑纳米药物通过Wnt信号通路激活用于蛋氨酸代谢免疫疗法

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、metabolic、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Honglin Tang ; Xiaojie Xu ; Lilong Liu ; Silu Tan ; Chongzhi Wu ; Zijian Shen ; Bowen Li ; Tingting Yuan ; Da Li ; Shipeng Ning ; Yuan PingSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTumor cells often outcompete T cells for methionine, impairing T cell function and immune surveillance. However, selectively targeting methionine metabolism in tumors remains challenging. Here, we develop a Wnt-activated RNA editing nanoplatform (TREND) to specifically disrupt the tumor methionine transporter SLC43A2 and reprogram the metabolic competition between tumor cells and CD8+ T cells. By taking advantages of aberrant Wnt signaling pathway in tumor cells, we first established a Wnt-responsive promoter which was used to control the transcription of the plasmid encoding RNA editor (CasRx) targeting SLC43A2, in order to ensure RNA editing in tumor cells with activated Wnt signaling. To further promote the accumulation and the intracellular translocation of CasRx in the tumor cells in vivo, a tumor-targeted delivery system was engineered by cloaking hybrid cell membrane over the polymeric carriers for the systemic delivery of CasRx plasmid. Such a therapeutic strategy combining tumor-targeted delivery and tumor-specific RNA editing greatly relieves the metabolic competition of methionine between tumor cells and T cells, restores H3K79me2 and STAT5 expression and increases intracellular glutathione (GSH) to suppress ROS-driven activation of the NFAT/NR4a/Tox exhaustion axis, thereby reducing immune checkpoint expression. This strategy significantly boosts the activity of T-cell effectors and suppresses the progression of tumors in multiple mouse models, providing a modular and programmable RNA-based approach for tumor-targeted metabolic immunotherapy.
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3. ⭐ GSE284607 洛尼达明可减轻嗜酸性慢性鼻窦炎小鼠模型中的炎症和组织重塑：一项单细胞转录组学研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、single-cell、transcriptomics
• 📝 描述：Contributor : Yicheng XieSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe performed single-cell sequencing on the mice nasal mucosal tissues of Control group, ECRS model group induced by papain (ECRS) and LND treatment group (LND).
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4. ⭐ GSE245825 扩张型心肌病中的心肌纤维化：转录组学见解、组织学相关性和类器官模型验证 [RNA-seq I]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac、RNA-seq、transcriptomics
• 📝 描述：Contributors : Reo Hata ; Yoshinori YoshidaSeries Type : Expression profiling by high throughput sequencing ; Third-party reanalysisOrganism : Homo sapiensDilated cardiomyopathy (DCM) represents a leading cause of heart failure among younger adults. Despite endomyocardial biopsy (EMB) transcriptome enriching our understanding of DCM, the link between its gene expression and phenotype remains unclear. RNA-seq analysis of 58 DCM samples and 12 publicly available control samples unveiled about 25,000 transcripts. A principal component analysis highlighted a distinct DCM-control separation. WGCNA revealed four transcriptome modules strongly associated with DCM. The purple module, which is the DCM-related module, was enriched with fibrosis-related genes and showed FSTL3 as a pivotal DCM-associated gene.
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5. ⭐ GSE300038 脂肪细胞在塑造大网膜卵巢癌肿瘤微环境中并非必需

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment
• 📝 描述：Contributors : Rachel L Mintz ; Jichang Han ; Emily G Butka ; Alexandre Gallerand ; Ayoung Kim ; Sarah Ning ; Nicole K Yiew ; Mary Wohltmann ; Wei Zou ; Nan Zhang ; Karen E Inouye ; Gökhan S Hotamişligil ; Samantha A Morris ; Bernd H Zinselmeyer ; Gwendalyn J RandolphSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe omentum, a specialized adipose tissue within the peritoneum, is a key metastatic niche for ovarian cancer (OC) dissemination during peritoneal carcinomatosis. The prevailing view is that omental adipocytes promote tumor growth by providinglipids, since global FABP4 deficiency curbs tumor growth. Here, we generated mice lacking mature adipocytes in the peritoneum and omentum. ID8p53–/–Brca2–/– , BPPNM, and KPCA OC cells retained a propensity to seed at regions typically associated with adipocytes, even without mature adipocytes. However, lack of mature adipocytes did not suppress peritoneal OC expansion, whereas removing the adipocyte-free omentum did. Murine and human single-cell RNA sequencing analysis revealed that endothelial FABP4 was high in the omentum. Indeed, endothelial cell-selective deficiency of FABP4 reduced OC growth in the peritoneum. These findings prompt a re-evaluation of adipocyte contributions to OC progression and point to a key role of the omental vasculature in supporting OC growth metabolically.
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6. ⭐ GSE304945 肿瘤来源的ADAMTSL4通过TGFβ信号通路驱动癌症恶病质

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、pathway
• 📝 描述：Contributors : Juliano Machado ; Vignesh Karthikaisamy ; Pia Benedikt-Kuehnast ; Doris Kaltenecker ; Pauline Morigny ; Amit Mhamane ; Julia Geppert ; Lisa Mehr ; Hermine Mohr ; Estefania S Fernandes ; Joanna D Lima ; Anastasia Georgiadi ; Chris D Hermann ; Achim Krüger ; Jose P Otoch ; Marc E Martignoni ; Inka Zörnig ; Julia Szendrödi ; Marilia Seelaender ; Olga Prokopchuk ; Maria Rohm ; Stephan Herzig ; Mauricio B DiazSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCancer cachexia (CCx) is a multifactorial wasting disorder in patients with cancer characterized by involuntary body weight loss. Whereas CCx is associated with reduced quality of life and poor survival, no approved pharmacological intervention exists. Here we show that elevated circulating levels of the tumour-derived glycoprotein ADAMTSL4 were associated with weight loss in various preclinical CCx models as well as in cachectic patients with different cancers. ADAMTSL4 overexpression in non-cachexia-inducing tumour cells conferred cachexia-inducing properties upon exposure of cultured myocytes and adipocytes as well as implantation in mice. Reversely, genetic ADAMTSL4 deletion in cachexia-inducing cancer cells markedly repressed wasting phenotypes both in vitro and in vivo. Ligand-receptor capture technology identified the latency-associated peptide of TGF-β1 as ADAMTSL4 target on muscle cell surface. ADAMTSL4 mediated muscle atrophy and adipose tissue wasting through local TGF-β1 activation, sensitive to inhibition of TGFβR1 or knockdown of proTGF-β1. Given the conserved correlation between circulating ADAMTSL4 and skeletal muscle TGF pathway component expression in an independent human cancer patient cohort, our data suggest that blockade of ADAMTSL4 function represents a first rational approach towards efficient cancer cachexia pharmacotherapy.
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7. GSE328601 肌肉质膜渗漏过多会破坏细胞外基质含量并改变巨噬细胞介导的肌肉修复 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、scRNA
• 📝 描述：Contributors : GaHyun Lee ; Lauren Vaught ; Dorothy DeBiasse ; Alexis Demonbreun ; Elizabeth McNallySeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPlasma membrane repair is critical for tissue integrity, especially for elongated contractile muscle cells. Genetically-mediated defects in plasma membrane resealing produce persistent leak, leading to a disordered extracellular matrix. Loss of the membrane repair protein dysferlin slows sarcolemmal resealing and promotes excess leak. Annexin A6 is also implicated in sarcolemmal repair, forming repair caps at the site of membrane disruption. On its own, deletion of the gene for annexin A6, Anxa6, had little effect on muscle health. In contrast, combined loss of dysferlin and annexin A6 (DysfA6) generated muscle fibers with profoundly defective membrane leak. Strikingly, Anxa6 deletion in the context of loss of dystrophin (mdxA6) did not exacerbate muscle defects. The persistent membrane leak in DysfA6 muscle resulted in marked macrophage infiltration with disordered macrophage polarization. Injured muscle fibers were targets of macrophage efferocytosis. Loss of Anxa6 was associated with increased expression of annexins A1 and A2, both of which were heavily deposited into the extracellular matrix. In vitro, macrophages exposed to annexins A1 and A2 expressed increased Csf1, consistent with a model where excess leak results in annexins A1 and A2 in the extracellular matrix, where this protein composition elicits macrophage proliferation and efferocytosis.
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8. GSE314776 解码 3D 染色质结构揭示前列腺癌中分层基因调控背后的不同增强子类别 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq
• 📝 描述：Contributors : Huan Cao ; Zexun Wu ; Baixi Ji ; Seolyn Yang ; Leonardo Gonzalez-Smith ; Suhn RhieSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensBackground: The transcription process is controlled by non-coding regulatory elements, more than 70% of which are putative enhancers. These enhancers comprise over 600,000 regions and are marked by histone modifications. However, the mechanisms by which altered enhancers in cancer cooperate within the three-dimensional chromatin architecture to drive oncogenic programs remain poorly understood. Results: By integrating 201 H3K27ac ChIP seq datasets from prostate, we identify 3,216 high confidence prostate cancer-specific putative enhancers. Ultra high resolution chromatin interaction profiling by Region Capture Micro-C at a representative chr6q24.1 locus reveals that these enhancers form cancer specific, highly nested interactions with promoters that coalesce into a multi connected hub absent in normal prostate cells. CRISPR/Cas9 perturbations of these enhancers, examined one by one, distinguish enhancer classes within the hub. Deletion of a central enhancer collapses hub-wide enhancer activities and architecture, leading to the downregulation of target genes, impaired proliferation, and reduced clonogenic growth. In contrast, deletion of a redundant enhancer results in minimal transcriptional changes, as neighboring enhancers rescue cancer signaling through compensatory architectural rewiring that strengthens alternative enhancer-promoter interactions. We also observe that FOXA1, a pioneer transcription factor activated in prostate cancer, directly binds to these enhancers and regulates distinct enhancer classes, leading to varying degrees of chromatin accessibility and gene expression changes.Conclusions: These findings suggest that enhancers function in a coordinated manner, forming multi-connected cancer-specific chromatin interaction hubs, with distinct enhancer classes contributing differently to gene regulation. This study advances our ability to modulate gene expression in a cell type-specific manner, opening new avenues for precision therapies.
• 🔗 查看原文

9. GSE314775 解码 3D 染色质结构揭示前列腺癌中分层基因调控背后的不同增强子类别 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributors : Huan Cao ; Zexun Wu ; Baixi Ji ; Seolyn Yang ; Leonardo Gonzalez-Smith ; Suhn RhieSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: The transcription process is controlled by non-coding regulatory elements, more than 70% of which are putative enhancers. These enhancers comprise over 600,000 regions and are marked by histone modifications. However, the mechanisms by which altered enhancers in cancer cooperate within the three-dimensional chromatin architecture to drive oncogenic programs remain poorly understood. Results: By integrating 201 H3K27ac ChIP seq datasets from prostate, we identify 3,216 high confidence prostate cancer-specific putative enhancers. Ultra high resolution chromatin interaction profiling by Region Capture Micro-C at a representative chr6q24.1 locus reveals that these enhancers form cancer specific, highly nested interactions with promoters that coalesce into a multi connected hub absent in normal prostate cells. CRISPR/Cas9 perturbations of these enhancers, examined one by one, distinguish enhancer classes within the hub. Deletion of a central enhancer collapses hub-wide enhancer activities and architecture, leading to the downregulation of target genes, impaired proliferation, and reduced clonogenic growth. In contrast, deletion of a redundant enhancer results in minimal transcriptional changes, as neighboring enhancers rescue cancer signaling through compensatory architectural rewiring that strengthens alternative enhancer-promoter interactions. We also observe that FOXA1, a pioneer transcription factor activated in prostate cancer, directly binds to these enhancers and regulates distinct enhancer classes, leading to varying degrees of chromatin accessibility and gene expression changes.Conclusions: These findings suggest that enhancers function in a coordinated manner, forming multi-connected cancer-specific chromatin interaction hubs, with distinct enhancer classes contributing differently to gene regulation. This study advances our ability to modulate gene expression in a cell type-specific manner, opening new avenues for precision therapies.
• 🔗 查看原文

10. GSE314774 解码 3D 染色质结构揭示前列腺癌中分层基因调控背后的不同增强子类别 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ATAC-seq
• 📝 描述：Contributors : Huan Cao ; Zexun Wu ; Baixi Ji ; Seolyn Yang ; Leonardo Gonzalez-Smith ; Suhn RhieSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensBackground: The transcription process is controlled by non-coding regulatory elements, more than 70% of which are putative enhancers. These enhancers comprise over 600,000 regions and are marked by histone modifications. However, the mechanisms by which altered enhancers in cancer cooperate within the three-dimensional chromatin architecture to drive oncogenic programs remain poorly understood. Results: By integrating 201 H3K27ac ChIP seq datasets from prostate, we identify 3,216 high confidence prostate cancer-specific putative enhancers. Ultra high resolution chromatin interaction profiling by Region Capture Micro-C at a representative chr6q24.1 locus reveals that these enhancers form cancer specific, highly nested interactions with promoters that coalesce into a multi connected hub absent in normal prostate cells. CRISPR/Cas9 perturbations of these enhancers, examined one by one, distinguish enhancer classes within the hub. Deletion of a central enhancer collapses hub-wide enhancer activities and architecture, leading to the downregulation of target genes, impaired proliferation, and reduced clonogenic growth. In contrast, deletion of a redundant enhancer results in minimal transcriptional changes, as neighboring enhancers rescue cancer signaling through compensatory architectural rewiring that strengthens alternative enhancer-promoter interactions. We also observe that FOXA1, a pioneer transcription factor activated in prostate cancer, directly binds to these enhancers and regulates distinct enhancer classes, leading to varying degrees of chromatin accessibility and gene expression changes.Conclusions: These findings suggest that enhancers function in a coordinated manner, forming multi-connected cancer-specific chromatin interaction hubs, with distinct enhancer classes contributing differently to gene regulation. This study advances our ability to modulate gene expression in a cell type-specific manner, opening new avenues for precision therapies.
• 🔗 查看原文

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1. Bioconductor 维护器验证

• ✍️ 作者：未知作者
• 🏷️ 关键词：Bioconductor
• 📝 描述：Introduction Bioconductor policies include being an active and reachable maintainer. Maintainer emails in the DESCRIPTION of packages often go stale as maintainers change positions. There is also a necessity to have maintainers opt into Biocond… Continue reading: Bioconductor Maintainer Validation
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1. ⭐ 肿瘤微环境的单细胞图谱揭示了特化的免疫亚群

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、tumor microenvironment、single-cell
• 📝 描述：Advances in RNA sequencing and spatial transcriptomics are revealing complex tumor ecosystems and enabling AI-driven approaches to improve precision immunotherapy and cancer treatment design… The post Single-cell maps of the tumor microenvironment reveal specialized immune subsets appeared first on RNA-Seq Blog.
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2. 单细胞图谱揭示克罗恩病的新见解

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：Single-cell RNA sequencing of more than 1.1 million intestinal cells reveals inflammatory drivers, persistent epithelial changes, and new therapeutic targets in Crohn’s disease… The post Single-cell atlas reveals new insights into Crohn’s disease appeared first on RNA-Seq Blog.
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• GSE298379 跨模型空间和单细胞图谱揭示了骨桥蛋白在多囊肾病中的保守作用
• GSE335219 研究发现，对 RAS(ON) 多选择性抑制剂 daraxonrasib 产生耐药性，这指导了胰腺癌的合理联合治疗策略。
• GSE335196 通过 RNA 测序 (RNA-seq) 在心肌梗死诱发心房颤动的鼠模型中鉴定出左心房组织中的基因表达改变。
• GSE335181 患者和细胞系来源的高级别浆液性卵巢癌球体的空间转录组分析
• GSE335080 全基因组表征染色体外环状 DNA 及其在结肠癌发生和发展中的功能作用 [Circle-Map]
• GSE299953 奥密克戎亚系突破感染诱导的年龄相关免疫特征的单细胞组学分析
• GSE330697 运动训练可延缓人体肌肉的分子衰老，维持能量代谢并增强运动反应
• GSE295663 猪心脏中人类心血管祖细胞的时空转录组学研究发现 MIDKINE 是新生血管形成的正调控因子
• GSE335441 HCFC2 在人类结直肠癌细胞系中的敲低
• GSE326376 转录辅助因子 Tle3 调控驻留记忆 CD8+T 细胞分化 [RNA-seq]
• GSE326375 转录辅助因子 Tle3 调控驻留记忆 CD8+T 细胞分化 [scRNA-seq]
• GSE326374 转录辅助因子 Tle3 调控驻留记忆 CD8+T 细胞分化 [ChIP-seq]
• GSE326373 转录辅助因子 Tle3 调控驻留记忆 CD8+T 细胞分化 [ATAC-seq]
• GSE314252 利用单核转录组学解码根瘤菌-番茄互作中的阶段特异性共生程序
• GSE301501 YAP/TAZ/TGF-β2轴介导的细胞外基质重编程驱动胆管癌模型中的免疫排斥
• GSE285108 SenCat：通过对多种衰老细胞类型进行多组学分析重新定义人类细胞衰老[scRNA-seq]
• GSE283043 RNA 结合蛋白 ZFP36L2 在小鼠中表现出组织选择性 mRNA 靶向性 [RNA-seq]
• GSE227456 基底膜蛋白在细胞外基质中表征NF1肿瘤的发生发展和对MEK抑制剂的反应
• GSE208712 WDR34 和 WDR60 功能缺失对 IMCD3 细胞转录组的影响
• GSE335290 piRNA通路中的发育转换确保果蝇中转座子沉默的阶段特异性
• GSE328583 肌肉细胞膜渗漏过多会破坏细胞外基质含量并改变巨噬细胞介导的肌肉修复
• GSE319177 研究发现，在创伤后应激障碍小鼠中，消退激活的前额叶-下丘脑通路编码积极情绪，以维持消退并防止复发。
• GSE318854 对来自患有特发性复发性流产 (RPLS) 患者的胎盘组织中的人类滋养层干细胞 (人类 TSC) 进行全球转录组分析。
• GSE314777 解码三维染色质结构揭示前列腺癌中层级基因调控背后的不同增强子类别
• GSE306548 人类早期胎盘和特发性复发性流产样本的转录组分析
• GSE296759 阐明化疗对骨骼祖细胞的影响 [bulk ATAC-seq]
• GSE296758 阐明化疗对骨骼祖细胞的影响 [RNA-seq MSPC]
• GSE296757 阐明化疗对骨骼祖细胞的影响 [RNA-seq 成骨细胞]
• GSE296752 阐明化疗对骨骼祖细胞的影响 [scRNA-seq]
• GSE295665 CT27 人类 TSC 细胞在 PRMT1 敲低前后的单细胞 RNA 测序分析
• GSE278039：利用小鼠胚胎第7.5、8.5、10.5、11.5和12.5天胎盘进行单细胞RNA测序分析
• GSE335307 角质形成细胞内在 VISTA 缺失对小鼠表皮中紫外线诱导的 I 型干扰素和炎症基因表达的影响 [scRNA-seq]
• GSE335237 高渗应激诱导 3D 染色质相互作用的大规模重组 [RNA-seq]
• GSE335225 RNA-seq 分析刺五加苷 E 处理的 MASH 小鼠肝脏
• GSE335221 角质形成细胞内在 VISTA 缺失对小鼠表皮中紫外线诱导的 I 型干扰素和炎症基因表达的影响 [bulk RNA-seq]
• GSE335210 人类结肠癌细胞模型中的 SOX9-BAF 多组学分析
• GSE335168 DU145样本的表观基因组分析
• GSE335156 健康大鼠动脉血和静脉血中免疫细胞分布的差异
• GSE335124 Ythdf1缺陷型SVF衍生脂肪细胞的RNA测序分析
• GSE335066 树鼩睾丸和附睾在生殖期和非生殖期的转录组和小RNA图谱
• GSE334702 荷斯坦奶牛子宫内膜转录组反应与含17α-羟孕酮己酸酯制剂和孕酮的关系：一项探索性RNA测序分析
• GSE329845 代谢调控的趋同进化控制弓形虫的氧化还原适应
• GSE315782 通过蛋白质组学分析探索性鉴定乳腺癌患者紫杉醇诱导周围神经病变的候选生物标志物和分子致病因素
• GSE301612 小胶质细胞与内皮细胞的相互作用促进细菌性脑膜炎中炎症性血脑屏障破坏