详细内容（前10条）

1. ⭐ GSE298611 β-catenin突变型肝细胞癌中谷氨酰胺合成酶的缺失重塑谷氨酰胺代谢，促进免疫抑制性巨噬细胞的适应 [dataset1.Spatial.Transcriptomics]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、macrophage、metabolism、spatial、transcriptomics
• 📝 描述：Contributors : Evan R Dalgado ; Panari Patel ; Junyan Tao ; Yekaterina Krutsenko ; Silvia Liu ; Daniel Green ; Raghad Alzubali ; Brandon M Lehrich ; Jia-Jun Liu ; Tyler Yasaka ; Minakshi Poddar ; Sucha Singh ; Vik Meadows ; Aaron W Bell ; Aatur Singhi ; Satdarshan MongaSeries Type : OtherOrganism : Mus musculusRecent therapeutic strategies using immune checkpoint inhibitors (ICIs) to treat hepatocellular carcinoma (HCC) have shown modest success. Response to ICIs is heterogeneous, and while mutational burden may predict stable responses, some HCCs with poor prognostic markers (e.g., CTNNB1 mutations) may still respond under favorable tumor immune microenvironment (TIME) conditions. We show that β-catenin-mutated HCCs lacking glutamine synthetase (GS) exhibit aggressive disease due to altered glutamate/glutamine (Glu/Gln) availability, driving macrophage adaptation that promotes immunosuppression. Loss of HCC Glul (encoding GS) forces hepatic macrophages to redistribute effort from immunologic to metabolic functions. Notably, depleting macrophages in GS-deficient, β-catenin-mutant HCC models improves survival. Additionally, HCC GS loss results in macrophage GS overexpression that maintains mTOR signaling in tumors, which is targetable. These findings reveal a metabolic dynamic between HCCs and the TIME which suggests that metabolic profiling, including GS expression, may refine patient selection for ICI therapies and improve outcomes under current standards of care.
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2. ⭐ GSE300260 AMPK依赖的表观遗传代谢调控介导紫檀芪在肝细胞癌中的抗癌作用。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、carcinoma、metabolism、epigenetic
• 📝 描述：Contributors : Cayla Boycott ; Megan Beetch ; Katarzyna Lubecka-Gajewska ; Benjamin S Ramsey ; Sandra Torregrosa-Allen ; Bennett D Elzey ; Abigail Cox ; Nadia Atallah Lanman ; Aline de Conti ; Min Li ; Mario Ferruzzi ; Igor Pogribny ; Barbara Stefanska (corresponding author)Series Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusScope: Disrupted metabolism, often implicated in hepatocellular carcinoma (HCC), is linked to aberrant epigenetic patterns. Dietary polyphenols, including pterostilbene (PTS), have been demonstrated to remodel epigenetic landscapes and restore metabolic homeostasis by regulating the activity of AMP-activated protein kinase (AMPK), a protein recently shown to orchestrate a diverse set of networks to epigenetically mediate transcription. We therefore explored the mechanistic involvement of AMPK in the epigenetic effects of PTS in HCC. Methods and Results: We incorporated PTS into a choline-deficient amino acid defined HCC-inducing diet (CDAA) in male Fisher-344 rats and found significant attenuation in HCC development compared to CDAA alone. Transcriptomics by RNA-sequencing revealed PTS-upregulated targets, that were enriched in key metabolic processes, including the folate (Aldh1l1), methionine (Bhmt) and sarcosine (Dmdgh) cycles. PTS-mediated gene upregulation was linked to lower levels of histone H3-methylation at lysine 27 (H3K27me3) at gene promoters. Mechanistic studies in HCC HepG2 cells revealed that AMPK inhibition abolished epigenetic gene activation in response to PTS, which was accompanied by diminished binding of H3K27me3-demethylase KDM6A at promoters of PTS-target genes. Conclusion: Our findings provide evidence for new disease vulnerabilities that arise from epigenetic/metabolic changes and constitute novel opportunities for preventative and therapeutic success in HCC.
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3. ⭐ GSE290189 SHMT2 modulates the transcriptome and metabolism profiles to promote the tumor phenotypes of bladder cancer HT-1376 cells

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、metabolism、transcriptome
• 📝 描述：Contributors : Xiaobo Guo ; Gang LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBladder cancer (BLCA) is a common malignant tumor of the urinary system. The development and progression of BLCA are controlled by multiple regulatory molecules, which have not been widely investigated. In this study, we explored the functions and downstream targets of serine hydroxy methyltransferase 2 (SHMT2) by silencing its expression using small interference RNA (siSHMT2) in HT-1376 cells. Whole transcriptome and metabolism profiles were deeply analyzed to identify the molecular targets of SHMT2. We found that siSHMT2 significantly reduced the proliferation rate and altered the cell cycle stages of HT-1376 cells. Moreover, siSHMT2 can modulate the expression of hundreds of genes (DEGs), including 126 upregulated and 106 downregulated DEGs. We then found that the most significant DEGs were tightly associated with progression of cancers, including PTMA, HNRNPR, RAPH1, TRAF3IP1, CNBP, and PRR15. At the same time, the alternative splicing profile was also regulated by siSHMT2, including the skipped exon as the dominant AS types. Finally, we identified the differential metabolites (DMs), and found the metabolism profile was significantly regulated by siSHMT2. Besides the purine metabolism, we observed that valine, leucine and isoleucine biosynthesis and degradation, TCA cycle, and propanoate metabolism were among the top pathways of DMs. In summary, we highlight the important roles of SHMT2 in HT-1376 cells and identified its downstream molecular targets, which are associated with the development of BLCA and can be used as therapeutic targets of BLCA in future.
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4. ⭐ GSE298616 β-catenin突变型肝细胞癌中谷氨酰胺合成酶的缺失重塑谷氨酰胺代谢，促进免疫抑制性巨噬细胞的适应

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、macrophage、metabolism
• 📝 描述：Series Type : Other ; Expression profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
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5. ⭐ GSE298614 β-catenin突变肝细胞癌中谷氨酰胺合成酶的缺失重塑谷氨酰胺代谢，促进免疫抑制性巨噬细胞的适应 [dataset3.scRNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、macrophage、metabolism
• 📝 描述：Contributors : Evan R Dalgado ; Panari Patel ; Junyan Tao ; Yekaterina Krutsenko ; Silvia Liu ; Daniel Green ; Raghad Alzubali ; Brandon M Lehrich ; Jia-Jun Liu ; Tyler Yasaka ; Minakshi Poddar ; Sucha Singh ; Vik Meadows ; Aaron W Bell ; Aatur Singhi ; Satdarshan MongaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusRecent therapeutic strategies using immune checkpoint inhibitors (ICIs) to treat hepatocellular carcinoma (HCC) have shown modest success. Response to ICIs is heterogeneous, and while mutational burden may predict stable responses, some HCCs with poor prognostic markers (e.g., CTNNB1 mutations) may still respond under favorable tumor immune microenvironment (TIME) conditions. We show that β-catenin-mutated HCCs lacking glutamine synthetase (GS) exhibit aggressive disease due to altered glutamate/glutamine (Glu/Gln) availability, driving macrophage adaptation that promotes immunosuppression. Loss of HCC Glul (encoding GS) forces hepatic macrophages to redistribute effort from immunologic to metabolic functions. Notably, depleting macrophages in GS-deficient, β-catenin-mutant HCC models improves survival. Additionally, HCC GS loss results in macrophage GS overexpression that maintains mTOR signaling in tumors, which is targetable. These findings reveal a metabolic dynamic between HCCs and the TIME which suggests that metabolic profiling, including GS expression, may refine patient selection for ICI therapies and improve outcomes under current standards of care.
• 🔗 查看原文

6. ⭐ GSE298613 β-catenin突变肝细胞癌中谷氨酰胺合成酶的缺失重塑谷氨酰胺代谢，促进免疫抑制性巨噬细胞的适应 [dataset2.scRNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、macrophage、metabolism
• 📝 描述：Contributors : Evan R Dalgado ; Panari Patel ; Junyan Tao ; Yekaterina Krutsenko ; Silvia Liu ; Daniel Green ; Raghad Alzubali ; Brandon M Lehrich ; Jia-Jun Liu ; Tyler Yasaka ; Minakshi Poddar ; Sucha Singh ; Vik Meadows ; Aaron W Bell ; Aatur Singhi ; Satdarshan MongaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusRecent therapeutic strategies using immune checkpoint inhibitors (ICIs) to treat hepatocellular carcinoma (HCC) have shown modest success. Response to ICIs is heterogeneous, and while mutational burden may predict stable responses, some HCCs with poor prognostic markers (e.g., CTNNB1 mutations) may still respond under favorable tumor immune microenvironment (TIME) conditions. We show that β-catenin-mutated HCCs lacking glutamine synthetase (GS) exhibit aggressive disease due to altered glutamate/glutamine (Glu/Gln) availability, driving macrophage adaptation that promotes immunosuppression. Loss of HCC Glul (encoding GS) forces hepatic macrophages to redistribute effort from immunologic to metabolic functions. Notably, depleting macrophages in GS-deficient, β-catenin-mutant HCC models improves survival. Additionally, HCC GS loss results in macrophage GS overexpression that maintains mTOR signaling in tumors, which is targetable. These findings reveal a metabolic dynamic between HCCs and the TIME which suggests that metabolic profiling, including GS expression, may refine patient selection for ICI therapies and improve outcomes under current standards of care.
• 🔗 查看原文

7. ⭐ GSE298111 GLMP通过激活自噬和RhoA通路促进非小细胞肺癌的EGFR-TKI耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、pathway
• 📝 描述：Contributors : Xiao Liang ; Jiali Xu ; Erbao Zhang ; Renhua GuoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHere, we report that the EGFR-TKI resistance mechanism is mediated by lysosome-related regulation. We established an osimertinib-resistant cell line, designated PC9OR, derived from the parental PC9 cells. The overexpression of glycosylated lysosomal membrane protein (GLMP) in PC9OR promotes resistance to Osimertinib. Mechanistically, GLMP could regulate the ubiquitination of RhoA and promote resistance by activating the epithelial-mesenchymal transition (EMT). Our findings provide a potential therapeutic strategy to overcome resistance to EGFR-TKIs.
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8. ⭐ GSE296966 雄激素受体促进 ER 突变乳腺癌中的线粒体氧化磷酸化、肉碱代谢和对棕榈酸脂毒性的抵抗。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolism、resistance
• 📝 描述：Contributors : Sessions Dane ; Spoelstra Nicole ; Caino Cecilia ; Yu Min ; Goodspeed Andrew ; Richer JenniferSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe effect of androgen receptor (AR) in ER+ breast cancer remains controversial. We find that AR promotes tumor cell growth, oxidative phosphorylation, and fatty acid oxidation under conditions mimicking long-term aromatase inhibition. AR also promotes expression of the mitochondrial and peroxisomal acylcarnitine synthesis enzyme CRAT. AR inhibition decreases CRAT expression and CRAT knockdown is sufficient to inhibit OXPHOS. AR inhibition does not elicit a broad anti-OXPHOS transcriptomic signature, but does affect the expression of a few key metabolic enzymes. AR antagonism also induces a metabolomic signature consistent with severe OXPHOS dysfunction. This work identifies AR as a regulator of CRAT and OXPHOS in ER+ breast cancer.
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9. ⭐ GSE313152 乳腺癌患者肺转移灶和正常肺组织的单细胞 RNA 测序。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、sequencing、single-cell
• 📝 描述：Contributors : C E Caldon ; Leila EshraghiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe estrogen receptor (ER) drives growth in most breast cancers. Endocrine therapy reduces recurrence, however around 30% of cancers relapse. Many recurrences occur years later, with slowly proliferating, hard-to-treat disease. To study this, we generated slow-growing resistant cells that form small primary tumours but readily metastasize. Single-cell RNA sequencing (scRNAseq) revealed that endocrine therapy reprograms these cells, notably upregulating the Rac1 signalling component P-Rex1. We found in clinical cohorts that P-Rex1 is high in ER+ breast cancer, including in late recurrent disease.
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10. ⭐ GSE255130 肠道菌群代谢产物吲哚-3-乙酸通过转录因子AHR维持肠道上皮稳态

• ✍️ 作者：未知作者
• 🏷️ 关键词：gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
• 📝 描述：Contributor : Mengfan LiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe incidence and prevalence of inflammatory bowel disease (IBD) is gradually increasing. A high-fat diet (HFD) is known to disrupt intestinal homeostasis and aggravate IBD, yet the underlying mechanisms remain largely undefined. Here, a positive correlation between dietary fat intake and disease severity in both IBD patients and HFD-fed mice is observed. HFD induces a significant decrease in indole-3-acetic acid (IAA) and lead to intestinal barrier damage. Furthermore, IAA supplementation enhances the intestinal mucin sulfation and effectively alleviates colitis. Mechanistically, IAA upregulates key molecules involved in mucin sulfation, including Papss2 and Slc35b3, the synthesis enzyme and the transferase of 3’-phosphoadenosine-5’-phosphosulfate (PAPS), via the Aryl Hydrocarbon Receptor (AHR). More importantly, AHR can directly bind to the transcription start site of Papss2. Oral administration of Lactobacillus reuteri, which can produce IAA, contributes to protecting against colitis and promoting mucin sulfation, while the modified L. reuteri strain lacking the iaaM gene (LactobacillusΔiaaM) and the ability to produce IAA fails to exhibit such effects. Overall, IAA enhances intestinal mucin sulfation through AHR, contributing to the protection of intestinal homeostasis.
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1. MUTE-Seq——一种检测低频癌症突变的超灵敏方法

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：MUTE-Seq enriches rare cancer mutations by removing wild-type DNA, enabling highly sensitive detection that enhances liquid biopsy..
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2. 血液检测显示，肥胖会迅速加速阿尔茨海默病的发展进程。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Obesity accelerates the rise of Alzheimer’s-related blood biomarkers far more rapidly than previously recognized. Long-term imaging and plasma data show that obese individuals experience much faster increases in proteins linked to neurodegeneration and amyloid buildup. Surprisingly, blood tests detected these changes earlier than PET scans. The results point to obesity as a major, modifiable contributor to Alzheimer’s progression.
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3. 科学家揭示癌症得以反弹的隐藏生存秘诀

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists discovered that certain cancer cells use a low-level activation of a DNA-dismantling enzyme—normally seen in cell death—to survive treatment. Instead of dying, these “persister cells” leverage this sublethal signal to regrow. Because the mechanism is non-genetic, it appears much earlier than typical resistance mutations. Targeting this enzyme could help stop tumors from returning.
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• GSE301532 C9orf72突变体和同源对照人iPSC衍生小胶质细胞的单细胞RNA测序
• GSE290095 2 型糖尿病冠状动脉微循环的空间转录组分析揭示了心脏不同区域的异质性 [scRNA-seq]
• GSE290094 2 型糖尿病冠状动脉微循环的空间转录组分析揭示了心脏不同区域的异质性 [Visium]
• GSE285383 CCL5 通过调节血小板驱动的 M2 巨噬细胞极化促进血管紧张素 II 诱导的心脏重塑
• GSE283015 Spatial immune landscape of large artery atherosclerotic and cardioembolic thrombus retrieved from mechanical thrombectomy
• GSE276026 RNA测序研究前列腺癌细胞中FZD6基因敲低的情况
• GSE312476 TRC-051384 激活热休克通路保护螺旋神经节神经元免受噪声引起的听力损失 [RNA-Seq]
• GSE174112 单细胞转录组揭示了哺乳仔猪和早期断奶仔猪回肠的异质性和不同状态
• GSE165094 桃果实全基因组亚硫酸氢盐测序
• GSE116645 全基因组DNA甲基化介导可变剪接转录本
• GSE109189 梨果实全基因组亚硫酸氢盐测序
• GSE109188 苹果果实全基因组亚硫酸氢盐测序
• GSE313098 时间序列 RNA-seq 分析揭示了慢性淋巴细胞白血病 (CLL) 自体和单培养体外模型中动态的转录反应和相互作用
• GSE310345 跨物种单细胞分析揭示线粒体功能障碍的性别差异是 Tau 病理的保守特征
• GSE307293 岩藻糖基转移酶 8 衍生的环状 RNA 通过 ENO1-TNF 信号通路驱动巨噬细胞 M2 极化，从而促进肺癌进展
• GSE305935 澳大利亚海湾战争老兵的免疫转录组变化
• GSE305134 RORB 在神经母细胞瘤细胞中的全基因组占位情况。
• GSE302840 RPL22 表达鉴定出 MLH1 缺陷型子宫内膜癌的一个转录亚群，该亚群影响肿瘤浸润淋巴细胞
• GSE302839 RPL22 表达鉴定出 MLH1 缺陷型子宫内膜癌的转录亚群，该亚群影响肿瘤浸润淋巴细胞 [蛋白质]
• GSE302749 RPL22 表达鉴定出 MLH1 缺陷型子宫内膜癌的转录亚群，该亚群影响肿瘤浸润淋巴细胞 [转录本]
• GSE299344 PARP 和 CLK/DYRK 抑制在耐药性高级别浆液性癌中的作用
• GSE297829 单细胞 RNA 测序揭示了接受透析 3 年患者腹膜微环境的动态变化，并为腹膜纤维化提供了新的见解。
• GSE296196 SIRPG以CD47非依赖性方式增强活化诱导的T细胞增殖
• GSE293768 VTC3 和 VTC2 对拟南芥光照下转录组的影响
• GSE287861 研究发现，关节软骨中 GATA4 水平的衰老相关性升高与软骨细胞再生能力受损和骨关节炎有关。
• GSE278347 CEBPB drives endothelial pathological phenotype and promotes atherosclerosis by directly upregulating TGFBR1 expression [RNA-seq]
• GSE278346 CEBPB 通过直接上调 TGFBR1 表达驱动内皮病理表型并促进动脉粥样硬化 [scRNA-seq]
• GSE313261 小鼠脾脏中IL-33、IL-25、IL-13、TSLP、IL-4和IL-9过表达的全局转录组分析
• GSE313259 Apoe3 通过 Lrp4 增强乙酰胆碱受体聚集
• GSE313176 Müller细胞谷氨酰胺代谢将糖尿病视网膜病变中的光感受器和内皮损伤联系起来
• GSE313146 上皮 miRNA 的上调与进行性支气管癌前病变中的免疫逃逸有关。
• GSE313145 上皮 miRNA 的上调与进行性支气管癌前病变中的免疫逃逸相关 [PCGA_miRNA_BX]
• GSE313144 上皮 miRNA 的上调与进行性支气管癌前病变中的免疫逃逸相关 [PCGA_miRNA_BR]
• GSE313043 单细胞转录组分析表明，脑出血期间接受 BAF312 治疗的患者 TNF 信号传导降低
• GSE291568 含SET结构域的蛋白质和HCF-1维持跨代表观遗传记忆
• GSE291081 Ly6G+Nur77+血管周围巨噬细胞启动肺部对过敏原的2型免疫反应
• GSE289548 Ly6G+Nur77+巨噬细胞启动肺部对过敏原的2型免疫反应
• GSE311370 小鼠视网膜神经节细胞的完整空间图谱揭示了密度和基因表达特化 [En face Retina]
• GSE311369 小鼠视网膜神经节细胞的完整空间图谱揭示了密度和基因表达特化 [RGC_CrossSection]
• GSE305119 Ly6G+Nur77+巨噬细胞启动肺部对过敏原的2型免疫反应
• GSE281797 肥胖代谢功能障碍相关脂肪肝患者肝脏活检的转录组学特征
• GSE310742 FABP4 是心血管疾病预后不良的标志物，它能诱导中性粒细胞产生促动脉粥样硬化的表型，而这种表型可被索玛鲁肽调节。
• GSE291990 Z-DNA 形成诱导全能性样状态并启动 Zscan4 依赖性染色质区室化 [scRNA-seq]
• GSE291987 Z-DNA 形成诱导全能样状态并启动 Zscan4 依赖的染色质区室化 [RNA-Seq]
• GSE291983 Z-DNA 形成诱导全能样状态并启动 Zscan4 依赖的染色质区室化 [Hi-C]
• GSE284076 tRNA 片段的转录后修饰赋予动脉粥样硬化中高密度脂蛋白功能改变 [小 RNA 测序]
• GSE284071 tRNA 片段的转录后修饰赋予动脉粥样硬化中高密度脂蛋白功能改变 [RNA-seq]
• GSE270833 核相分离驱动急性髓系白血病