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1. ⭐ GSE310689 AR 中的最小长度 CAG 重复序列定义了过度活跃的 AR-LSD1 轴，驱动前列腺癌的代谢重编程 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolic、RNA-seq
• 📝 描述：Contributors : Songqi Zhang ; Muqing Li ; Mingyu Liu ; Changmeng CaiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe polymorphic CAG trinucleotide repeat in the androgen receptor (AR) gene encodes a variable-length N-terminal polyglutamine (polyQ) tract that modulates AR transcriptional activity, with shorter tracts generally enhancing AR activity. While the majority of men harbor CAG repeats longer than 17, a small subset carry minimal-length CAG repeats (≤17) in AR. These alleles are primarily found in men of African ancestry (AA), accounting for over 10% of the population, and may significantly contribute to the increased prostate cancer (PCa) risk and worse clinical outcomes observed in AA men. However, how this distinct pattern of polymorphism influences AR-chromatin interaction, metabolic reprogramming, and therapeutic response remains unclear. Here, we established isogenic PCa cell lines harboring AR with a minimal length of CAG repeats that encode an ultrashort polyQ track and found that this AR variant exhibits resistance to AR-targeted therapy with markedly enhanced protein stability, expanded chromatin binding, and a reprogrammed transcriptional profile. Notably, the ultrashort polyQ AR also reshaped global FOXA1 occupancy and upregulated genes involved in fatty acid metabolism, lipid synthesis, and anaerobic glycolysis. Moreover, we identified a markedly increased AR-LSD1 interaction and showed that LSD1 inhibition suppressed this metabolic reprogramming and reduced tumor growth. Together, these findings define a hyperactive AR-LSD1 chromatin axis driven by minimal-length CAG repeats in AR and reveal a mechanistic link between inherited AR polymorphism, AR-mediated epigenetic–metabolic remodeling, and population-associated disparities in prostate cancer biology.
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2. ⭐ GSE310685 AR 中的最小长度 CAG 重复序列定义了过度活跃的 AR-LSD1 轴，驱动前列腺癌的代谢重编程 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolic、ChIP-seq
• 📝 描述：Contributors : Songqi Zhang ; Muqing Li ; Mingyu Liu ; Changmeng CaiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensThe polymorphic CAG trinucleotide repeat in the androgen receptor (AR) gene encodes a variable-length N-terminal polyglutamine (polyQ) tract that modulates AR transcriptional activity, with shorter tracts generally enhancing AR activity. While the majority of men harbor CAG repeats longer than 17, a small subset carry minimal-length CAG repeats (≤17) in AR. These alleles are primarily found in men of African ancestry (AA), accounting for over 10% of the population, and may significantly contribute to the increased prostate cancer (PCa) risk and worse clinical outcomes observed in AA men. However, how this distinct pattern of polymorphism influences AR-chromatin interaction, metabolic reprogramming, and therapeutic response remains unclear. Here, we established isogenic PCa cell lines harboring AR with a minimal length of CAG repeats that encode an ultrashort polyQ track and found that this AR variant exhibits resistance to AR-targeted therapy with markedly enhanced protein stability, expanded chromatin binding, and a reprogrammed transcriptional profile. Notably, the ultrashort polyQ AR also reshaped global FOXA1 occupancy and upregulated genes involved in fatty acid metabolism, lipid synthesis, and anaerobic glycolysis. Moreover, we identified a markedly increased AR-LSD1 interaction and showed that LSD1 inhibition suppressed this metabolic reprogramming and reduced tumor growth. Together, these findings define a hyperactive AR-LSD1 chromatin axis driven by minimal-length CAG repeats in AR and reveal a mechanistic link between inherited AR polymorphism, AR-mediated epigenetic–metabolic remodeling, and population-associated disparities in prostate cancer biology.
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3. GSE235461 p63 和 p73 通过高度重叠的转录程序协同促进皮肤鳞状细胞癌的发生 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、ChIP-seq
• 📝 描述：Contributors : Dario Antonini ; Marco Ferniani ; Claudia Russo ; Dania Al-Labban ; Jieqiong Qu ; Paola Ostano ; Marco Franciosi ; Ludovica D’Auria ; Andrew South ; Huiqing Zhou ; Madhavi Kadakia ; Caterina MisseroSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensAberrant expression of transcriptional regulators can affect oncogenic gene expression programs in cancer. Mutations in the tumor suppressor p53 are commonly found in UV-damaged skin and protect damaged epidermal cells from senescence and or oncogene-induced apoptosis, favoring cancer formation. In contrast, the other p53 family members p63 and p73 are rarely mutated in cancer and p63 is often amplified or overexpressed in lung, esophagus, and head and neck squamous cell carcinoma (SCC). Here, we demonstrate that both p63 and p73 are required for cell proliferation in epidermal cells and in skin SCC and are overexpressed in preneoplastic lesions and in skin SCCs. p63/p73 form heterotetramers and co-occupy thousands of regulatory regions, jointly controlling a transcriptional program that promotes cell proliferation and tumorigenesis. The combination of gene knockdown with transcriptomic and epigenetic analyses revealed that p63 and p73 control a transcriptional feed-forward circuit that sustains cell proliferation. We find that in skin SCC a key signaling pathway downstream of p63/p73 is the Epidermal Growth Factor Receptor (EGFR)/MAP kinase. p63/p73 directly and positively control transcription of the EGFR ligands, among which amphiregulin (AREG) is the most highly expressed in skin SCC. Like p63/p73, AREG is critical to maintain skin SCC proliferative potential, anchorage independent growth, and to promote tumorigenesis. Thus, p63 and p73 act as oncogenic drivers in skin SCC, with AREG being a crucial non-cell-autonomous effector downstream of p63 and p73 in skin SCC formation.
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4. GSE235459 p63 和 p73 通过高度重叠的转录程序协同促进皮肤鳞状细胞癌的发生 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、RNA-seq
• 📝 描述：Contributors : Dario Antonini ; Marco Ferniani ; Claudia Russo ; Dania Al-Labban ; Jieqiong Qu ; Paola Ostano ; Marco Franciosi ; Ludovica D’Auria ; Andrew South ; Huiqing Zhou ; Madhavi Kadakia ; Caterina MisseroSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAberrant expression of transcriptional regulators can affect oncogenic gene expression programs in cancer. Mutations in the tumor suppressor p53 are commonly found in UV-damaged skin and protect damaged epidermal cells from senescence and or oncogene-induced apoptosis, favoring cancer formation. In contrast, the other p53 family members p63 and p73 are rarely mutated in cancer and p63 is often amplified or overexpressed in lung, esophagus, and head and neck squamous cell carcinoma (SCC). Here, we demonstrate that both p63 and p73 are required for cell proliferation in epidermal cells and in skin SCC and are overexpressed in preneoplastic lesions and in skin SCCs. p63/p73 form heterotetramers and co-occupy thousands of regulatory regions, jointly controlling a transcriptional program that promotes cell proliferation and tumorigenesis. The combination of gene knockdown with transcriptomic and epigenetic analyses revealed that p63 and p73 control a transcriptional feed-forward circuit that sustains cell proliferation. We find that in skin SCC a key signaling pathway downstream of p63/p73 is the Epidermal Growth Factor Receptor (EGFR)/MAP kinase. p63/p73 directly and positively control transcription of the EGFR ligands, among which amphiregulin (AREG) is the most highly expressed in skin SCC. Like p63/p73, AREG is critical to maintain skin SCC proliferative potential, anchorage independent growth, and to promote tumorigenesis. Thus, p63 and p73 act as oncogenic drivers in skin SCC, with AREG being a crucial non-cell-autonomous effector downstream of p63 and p73 in skin SCC formation.
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5. GSE339080 视黄酸受体信号传导在早期妊娠期间协调子宫容受性、蜕膜功能和免疫稳态 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、scRNA
• 📝 描述：Contributors : Yan Yin ; Liang Ma ; David ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSingle-cell RNA sequencing was performed on uterine tissues collected from control and retinoic acid receptor triple-conditional knockout (tKO) female mice at 3.5 days post coitum. This study was designed to characterize changes in uterine cellular composition and gene-expression programs associated with loss of RAR signaling during the implantation period. The dataset provides transcriptomic profiles of different uterine cell populations and enables comparison of cell-type-specific responses between control and tKO uteri.
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6. GSE338522 DNMT1-核小体复合物的结构揭示了CpG岛中DNA甲基化和调控的维持基础[RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、methylation
• 📝 描述：Contributors : Gang Greg Wang ; Bo PanSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDNA methylation is an important epigenetic mechanism that is essential for genomic stability and gene regulation. In mammals, DNA methyltransferase DNMT1 plays a critical role in maintaining the DNA methylation landscape during development. However, how DNMT1 interplays with various chromatin environments to shape the DNA methylation landscape across the genome remains unclear. Here we report the structure and regulation of DNMT1-mediated DNA methylation at the nucleosome level. Two clusters of previously underappreciated DNA-binding sites of DNMT1 engage in orthogonal nucleosomal contacts, in concert with the interaction between the DNMT1 RFTS domain and histone H3 carrying dual mono-ubiquitin, underpin DNMT1-mediated maintenance DNA methylation along the nucleosome core particle (NCP)-proximal linker. The interaction of DNMT1 CXXC domain with an unmodified CpG site leads to an autoinhibitory conformation of DNMT1 during the encounter stage, and further allosterically inhibits DNMT1-mediated maintenance DNA methylation at the stage of productive methylation. Introducing a DNMT1 mutation defective in the CXXC-CpG interaction substantially increased the DNA methylation of CpG islands (CGIs) without impacting the overall genomic methylation appreciably, suggesting a CXXC domain-dependent rheostat mechanism restricting DNA methylation in the CGIs associated with vertebrate genomes. Together, this study provides insight into the interplay between the conformational dynamics of DNMT1 and the chromatin environment-guided DNA methylation.
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7. GSE336655 逻辑门控合成电路结合微环境重编程克服抗原贫乏软骨肉瘤的免疫排斥

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、antigen
• 📝 描述：Contributors : Jooyeon Suh ; Geunho Yook ; Jin-Hong KimSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChondrosarcoma (CHS) remains refractory to immunotherapy due to a paucity of targetable-antigen and a suppressive tumor microenvironment (TME). We developed a modular strategy integrating tumor-intrinsic genetic logic with rational TME reprogramming to overcome these barriers. Using a 57,715-element massively parallel reporter assay (MPRA), we identified CHS-selective synthetic promoters and engineered a Boolean AND-gate circuit that ensures high-fidelity expression of a surface T-cell engager (STE) exclusively within malignant cells. To further resolve the immunosuppressive TME, we identified macrophage migration inhibitory factor (MIF) as a blockade target. Single-cell RNA sequencing in human-PBMC-reconstituted CHS-xenograft models revealed that the circuit initiates T-cell activation, while MIF blockade prevents exhaustion by promoting proliferative T-cells and M1-polarized macrophages. Local administration induced a systemic abscopal effect, regressing distant, untreated tumors. Collectively, these findings provide a programmable blueprint for converting immunologically cold, antigen-poor malignancies into systemically immune-responsive states.
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8. GSE313369 内皮细胞周期抑制可促进血管成熟，使肿瘤血管系统正常化 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、scRNA
• 📝 描述：Contributors : Shelby R Cain ; Gael Genet ; Nafiisha Genet ; Jordan W Aragon ; Madeline G Jackson ; Umadevi Paila ; Nicholas W Chavkin ; Karen HirschiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDysfunctional tumor vessels promote disease progression, and improving vessel function enhances delivery of therapeutics. However, current approaches to normalize the tumor vasculature have limited efficacy. Palbociclib, an FDA-approved cyclin-dependent kinase 4/6 inhibitor (CDK4/6i) has beneficial effects on tumor and immune cells, but its impact on tumor vasculature is unknown. In our studies, murine mammary tumor ECs (TECs) exhibited disrupted cell cycle control and impaired specification, and CDK4/6i treatment promoted TEC cycle control, enabling improved tumor vascular structure and function. To gain mechanistic insight, we performed scRNAseq that showed CDK4/6i-mediated TEC cycle arrest promoted arterial-venous specification, EC junctions, and pericyte recruitment, and suppressed genes regulating glycolysis and immunosuppressive signaling. These effects were associated with increased vessel perfusion, decreased tumor hypoxia, and enhanced anti-PD-1 immunotherapy.
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9. GSE331378：用二价BET溴结构域抑制剂MS645或单价抑制剂JQ1治疗后，对PC3来源的人类前列腺癌异种移植瘤和匹配的小鼠血液进行批量RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributors : Yifei Sun ; Qiangmin Zhang ; Anbalagan Jaganathan ; Kunhong Xiao ; Ming-Ming ZhouSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusMale ICR SCID mice (5-6 weeks old) were implanted subcutaneously with 5 x 10^6 PC3 cells. When tumors reached ~200 mm^3, mice were randomized to one of three treatment arms: vehicle, JQ1 (30 mg/kg), or MS645 (20 mg/kg). Compounds were administered intraperitoneally. At study end, mice were sacrificed and matched xenograft tumor and whole-blood specimens were collected and snap-frozen for bulk RNA-seq. Tumor RNA-seq reads were aligned to the human reference genome (GRCh38/hg38) and blood RNA-seq reads to the mouse reference genome (GRCm38/mm10). Differential expression analysis (DESeq2) was used to compare MS645 vs vehicle and JQ1 vs vehicle in each compartment. The study identifies the BRD4-RUVBL1/2 axis as a mediator of intrinsic resistance to monovalent BET bromodomain inhibition in AR-negative prostate cancer and demonstrates that bivalent BET targeting by MS645 reprograms resistant tumors toward a treatment-responsive transcriptional state.
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10. GSE307400 基于单细胞测序数据，探索与人类免疫缺陷病毒感染引起的股骨头坏死相关的关​​键细胞和基因

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributor : Gaorui CaiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Human immunodeficiency virus (HIV)-associated Acquired immunodeficiency syndrome (AIDS), a global public health challenge, is managed by Highly active antiretroviral therapy, though long-term use is linked to chronic complications. Osteonecrosis of the femoral head (ONFH), a prevalent HIV-associated disorder with complex etiology, remains mechanistically unclear. Single-cell RNA sequencing (scRNA-seq) offers novel insights into HIV-ONFH pathogenesis. Methods: In this study, femoral head tissue and bone marrow samples from HIV-ONFH and femoral neck fracture patients underwent single-cell sequencing. Data processing involved Seurat for quality control, identification of highly variable genes, dimensionality reduction, clustering, and cell annotation. Enrichment analyses utilized ReactomeGSEA and gene set variation analysis (GSVA), while key genes were selected via protein-protein interaction (PPI) network construction with CytoHubba algorithms. Subsequent analyses included key gene characterization, molecular regulatory network construction, drug prediction, molecular docking, and single-cell expression profiling via Seurat and Monocle. Results: Key cell types in ONFH were identified, with CD8+ T cells as critical effectors. Single-cell analysis revealed their heterogeneity and communication patterns. Twenty-nine candidate genes were prioritized via PPI network analysis, enriched in pathways like MAPK signaling. Four hub genes (HNRNPU, RPS4Y1, RPS9, RPL35) were validated with chromosomal (Chr1, 9, 19, Y) and subcellular localizations (nucleus, extracellular, cytoplasm), exhibiting ribosomal/physical interaction functions. Molecular regulatory network analysis identified 28 key transcription factors (e.g., hsa-miR-3142, AL_355075_4) driving cell-type-specific modules. Drug-docking simulations revealed high-affinity interactions (CYCLOHEXIMIDE w/RPL35/RPS9: -5.6/-6.6 kcal/mol; ATALUREN w/RPS4Y1: -7.1 kcal/mol). Gender-specific expression patterns and differentiation-dependent trends were observed, with ETS2/CEBPA identified as master regulators in CD8+ subsets. Conclusion: This study analyzed targeted therapeutic genes and molecular mechanisms of HIV-ONFH, linked CD8+ T cell-related genes to the disease, and provided a scientific basis for precise interventions. However, results require further validation by subsequent research.
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1. 您需要定制的 R 包或 Shiny 应用吗？我可以为您开发。

• ✍️ 作者：未知作者
• 🏷️ 关键词：R package
• 📝 描述：I offer turning a set of requirements into a maintainable package or dashboard Continue reading: Do you need a custom R package or Shiny app? I can build it for you
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1. ⭐ SPIDER利用单细胞RNA测序改进空间转录组学数据

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：SPIDER uses single-cell RNA sequencing references to reduce noise in spatial transcriptomics, improving gene expression patterns, tissue structure identification…
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2. CellTypeAI – 使用本地生成 AI 进行 scRNA-seq 的细胞注释

• ✍️ 作者：未知作者
• 🏷️ 关键词：scRNA
• 📝 描述：CellTypeAI combines local generative AI with biological context to improve cell annotation accuracy in single-cell RNA sequencing while helping researchers keep sensitive data private…
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• GSE296281：Hes1基因在肺泡上皮细胞特异性缺失后的单细胞RNA测序分析
• GSE324830 体内 CRISPR 筛选发现 NF1/RASA1/TP53 共突变及其下游 MEK 信号通路是鼻窦肿瘤发生的常见关键机制 - Nf1/Trp53 flox/flox 的全外显子组测序
• GSE317815 SNORD104 指导的 rRNA 甲基化缺失促进肺腺癌对克唑替尼的早期适应
• GSE305281 异常上皮化：子宫内膜息肉发生的可能因素 [scRNA-seq]
• GSE305280 异常上皮化：子宫内膜息肉发生的可能因素 [批量 RNA 测序]
• GSE303511 体内 CRISPR 筛选发现 NF1/RASA1/TP53 共突变和下游 MEK 信号通路是鼻窦肿瘤发生的常见关键机制 - CRISPR Cas9 定制捕获测序
• GSE284284 动态 Polycomb-CBC 串扰协调植物转录活跃位点的 mRNA 产生 [ChIP-seq]
• GSE345436 人类遗传学表明 BACH2-NRF2 轴参与胎儿血红蛋白活化 [RNA-Seq]
• GSE345415 线粒体丙酮酸载体在肝星状细胞活化中的关键作用 [scRNA-Seq]
• GSE322492 视黄酸受体信号传导在妊娠早期协调子宫容受性、蜕膜功能和免疫稳态
• GSE314435 大规模RNA结合蛋白锚定筛选发现环状RNA代谢的调节因子
• GSE314434 大规模 RNA 结合蛋白系链筛选发现环状 RNA 代谢的调节因子 [tethering_screen_fly_total_RNA_seqs]
• GSE314433 大规模 RNA 结合蛋白系链筛选发现环状 RNA 代谢的调节因子 [tethering_screen_RBM15_OE_KD_total_RNA_seq]
• GSE314432 大规模 RNA 结合蛋白系链筛选发现环状 RNA 代谢的调节因子 [tethering_screen_LARP4B_RIP_eCLIP]
• GSE314431 大规模 RNA 结合蛋白系链筛选发现环状 RNA 代谢的调节因子 [tethering_screen_ribo_rna-seq]
• GSE313493 内皮细胞周期抑制可促进血管成熟，使肿瘤血管系统正常化 [bulkRNA-seq]
• GSE287140 DNMT1-核小体复合物的结构揭示了CpG岛中DNA甲基化和调控的维持基础[亚硫酸氢盐测序]
• GSE287117 DNMT1-核小体复合物的结构揭示了CpG岛中DNA甲基化和调控的维持基础[CUT&Tag]
• GSE277896 大规模 RNA 结合蛋白系链筛选发现环状 RNA 代谢的调节因子 [screen_BY]
• GSE235467 p63 和 p73 通过高度重叠的转录程序协同促进皮肤鳞状细胞癌的发生
• GSE345429 色素沉着加剧了急性皮肤炎症小鼠模型中的组织破坏并改变了转录组谱
• GSE344886 RNA-seq 分析贝伐珠单抗治疗的人类胶质母细胞瘤细胞系样本
• GSE344799 AML 和 ALL 细胞系的 RNA 测序
• GSE315408 空间和单核多组学分析揭示心内膜弹力纤维增生症中内皮细胞异质性过度增生 [MERFISH]
• GSE311511 空间和单核多组学分析揭示心内膜弹力纤维增生症中内皮细胞异质性过度增殖
• GSE307202 雄激素受体前体mRNA茎环结构决定前列腺癌中AR-V7的剪接命运
• GSE242111 利用mRNA技术局部递送SBRT和IL-12克服抑制屏障，消除胰腺癌