详细内容（全部9条）

1. ⭐ GSE316007 单细胞测序和空间转录组学研究表明，凝聚层-细胞-药物系统能有效保护骨关节炎大鼠的关节软骨免受磨损和退行性变质。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Sirong Chen ; Tianshen Jiang ; Pengchao Zhao ; Liming BianSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Rattus norvegicusWe employed DNBSEQ technology to perform single-cell RNA sequencing of rat macrophages, as well as single-cell and spatial transcriptomic analyses of rat knee joint tissues. Single-cell profiling of macrophages demonstrated that the coacervate–cell–drug system effectively reversed the pro-inflammatory phenotype by driving the transition of M1 macrophages toward a reparative M2c phenotype. Single-cell analysis of joint tissues further revealed strong interactions between exogenous GFP-labeled stem cells delivered by the coacervate–cell–drug system and endogenous joint-resident cells. Spatial transcriptomic analysis demonstrated that the coacervate–cell–drug system effectively promotes extracellular matrix repair in osteoarthritic cartilage.
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2. ⭐ GSE322775 KRAS抑制后协同免疫激活揭示了增强和限制抗肿瘤免疫的分子通路

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、immunity、KRAS
• 📝 描述：Contributors : Daniel Lu ; Tao Osgood ; Chi-Ming Li ; Matt KankeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWhile mutant-specific KRAS inhibitors are approved to treat cancer, a deeper understanding of intratumoral changes driven specifically by KRAS inhibition is needed to maximize therapeutic responses. Here we apply single-cell RNA-seq, flow cytometry, and spatial transcriptomics to distinguish mechanisms of tumor control after KRASG12C inhibition (KRAS(G12C)i), MEK inhibition (MEKi) and following combination therapy with KRAS(G12C)i and PD-1 blockade. Despite inhibiting overlapping pathways, KRAS(G12C)i drives the adaptation of distinct neoplastic cell fates affecting metabolism and cell cycle regulation, leading to synergistic tumor suppression after co-administration with MEKi. In turn, this modulates intercellular communication patterns and induces robust dendritic cell maturation and PD-1+ macrophage activation mediated through non-immune mediators. Both KRAS(G12C)i and MEKi elicit a similar magnitude of cytotoxic T-cell infiltration despite a reduced capacity for T-cell proliferation after MEKi, implicating distinct adaptive immune activation mechanisms. Combination treatment of KRAS(G12C)i with anti-PD-1 overcomes immune activation barriers by prolonging the activation window and clonal persistence for T cells and by promoting the re-wiring of pro-inflammatory macrophages associated with higher survival, Furthermore, combination treatment amplifies intercellular communication among non-PD-1+ expressing cells to perpetuate dendritic cell activation. Our findings connect neoplastic KRAS inhibition with the coordination of distinct levers for immune activation and reveal pro- and anti-tumor mechanisms that can be modulated following specific treatment types to contain malignant growth.
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3. GSE332655 SF3A3 通过 Notch 信号通路调控肝细胞癌细胞的增殖和迁移能力

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、pathway
• 📝 描述：Contributor : LiYing LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis study aims to investigate the expression, biological function, and molecular mechanism of the splicing factor SF3A3 in hepatocellular carcinoma (HCC). Analysis of the TCGA-LIHC cohort revealed that SF3A3 is significantly upregulated in HCC tissues and its high expression correlates with poor overall survival. We established SF3A3 knockdown and overexpression models in HepG2 and Huh7 cells. Functional assays (CCK-8, colony formation, EdU, wound healing, flow cytometry for cell cycle and apoptosis) demonstrated that SF3A3 overexpression promotes HCC cell proliferation and migration, whereas knockdown exerts opposite effects. To explore the underlying mechanism, we performed transcriptome sequencing (RNA-seq) on SF3A3-depleted HCC cells. Combined with bioinformatic analysis and validation using the GEO dataset GSE287381, we identified the Notch signaling pathway as a key target of SF3A3. Western blotting confirmed that SF3A3 knockdown reduces Notch1 and HES1 protein levels, while overexpression increases them. Collectively, our findings indicate that SF3A3 promotes HCC cell proliferation and migration by activating the Notch signaling pathway, providing a rationale for targeting the SF3A3-Notch axis in HCC therapy.
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4. GSE336234：对正常饮食组和高脂饮食组小鼠腹腔免疫细胞进行单细胞RNA测序分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、scRNA
• 📝 描述：Contributors : Weixuan Wang ; Linjiang Han ; Dan LvSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusTo determine how a high-fat diet (HFD) alters peritoneal immune cells, we performed single-cell RNA sequencing (scRNA-seq) to characterize the peritoneal immune microenvironment in mice fed a chow diet (CD) or HFD.
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5. GSE300955 IL4I1 和 LAO1 双重缺乏通过破坏 L-氨基酸代谢和 IDO1-犬尿氨酸途径促进炎症性腹泻

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、pathway
• 📝 描述：Contributors : Kentaro Nagaoka ; Hong LiuSeries Type : Expression profiling by arrayOrganism : Mus musculusThe oxidoreductases interleukin 4-induced gene 1 (IL4I1) and L-Amino acid oxidase 1 (LAO) are known to catalyze L-amino acid metabolism, yet their physiological roles in intestinal homeostasis remain largely unexplored. In this study, we investigated the impact of IL4I1 and LAO1 deficiency on colonic inflammation by generating wild-type, single knockout (IL4I1 KO and LAO1 KO), and double knockout (DKO) mice. Notably, DKO mice exhibited spontaneous diarrhea and histologically confirmed colitis, which were absent or rare in the other genotypes. Transcriptomic profiling and qRT-PCR analyses revealed upregulated expression of pro-inflammatory cytokines (IL-6, IL-17, IFN-γ) and Th1/Th17 transcription factors, along with overexpression of indoleamine 2,3-dioxygenase 1 (IDO1) in the colon of DKO mice. Metabolomic analysis indicated elevated colonic kynurenine levels and impaired metabolism of L-phenylalanine, L-tyrosine, and L-tryptophan. These changes were associated with a significant reduction in hydrogen peroxide (H₂O₂) production. Furthermore, 16S rRNA gene sequencing revealed altered beta diversity and reduced abundance of Short-chain fatty acid-producing bacteria in DKO mice. Among short-chain fatty acids, pentanoate was significantly decreased in DKO cecal contents. Collectively, these findings suggest that IL4I1 and LAO1 are essential for maintaining intestinal immune and metabolic balance. Their combined deficiency disrupts L-amino acid metabolism and H₂O₂-mediated regulation of the IDO1–kynurenine pathway, ultimately promoting gut dysbiosis and inflammatory diarrhea. This study provides novel insights into the metabolic and microbial mechanisms underlying colonic inflammation and highlights IL4I1 and LAO1 as potential targets for therapeutic intervention in inflammatory bowel diseases.This study provides novel insights into the metabolic and microbial mechanisms underlying colonic inflammation and highlights IL4I1 and LAO1 as potential targets for therapeutic intervention in inflammatory bowel diseases.
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6. GSE336483 应激应对表型塑造脂肪组织功能和可塑性并调节代谢弹性

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic
• 📝 描述：Contributors : Saumya Mehta ; Michaella Ben-Shachar ; Sharmila Govindaraj ; Suparna Sen ; Adrian Segev ; Oshrit Rahimi ; Valid Gahramanov ; Galia Luboshits ; Michael A Firer ; Ayala Wollman ; Albert Pinhasov ; Tovit RosenzweigSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis study investigated how stress-coping phenotypes (stress-resilient Dominant and stress-vulnerable Submissive mice) shape white adipose tissue (WAT) function under standard and high-fat diet (HFD) conditions. Metabolic, molecular, and transcriptomic analyses were performed on epididymal (eWAT) and inguinal (iWAT) white adipose tissue. Results revealed that stress-vulnerable mice exhibit impaired adipogenesis, adipocyte hypertrophy, unfavorable adipokine profiles, and defective insulin signaling in WAT under HFD. Transcriptomic profiling by RNA-seq identified adipogenesis, fatty acid metabolism, and oxidative phosphorylation as differentially regulated pathways between the strains. Functional analyses confirmed reduced proliferative and adipogenic potential of stromal vascular fraction (SVF) cells from stress-vulnerable mice. Pharmacological activation of PPARgamma (pioglitazone) improved adipogenesis and metabolic parameters, while antidepressant treatment (paroxetine) normalized behavioral deficits and improved adipogenic capacity in stress-vulnerable mice.
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7. GSE336205 DUSP5 通过 ERK1/2 下调 SCD1 表达来调控胰腺癌中的铁死亡

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis study aimed to explore the role and mechanism of DUSP5 in pancreatic ductal adenocarcinoma (PDAC). RNA sequencing was performed in DUSP5-overexpressing PANC-1 cells and control cells to identify differentially expressed genes. The results revealed that DUSP5 significantly downregulated stearoyl-CoA desaturase 1 (SCD1), a key enzyme involved in fatty acid metabolism and ferroptosis regulation. Our findings indicate that DUSP5 promotes ferroptosis and suppresses PDAC proliferation through the ERK1/2-SCD1 signaling pathway.
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8. GSE336175 代谢应激诱导的星形胶质细胞衰老和神经毒性是由 LRRK2-G2019S 驱动的，并且可通过 LED 光生物调节逆转

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic
• 📝 描述：Contributors : Jeehoon Lee ; Jihye HanSeries Type : Expression profiling by arrayOrganism : Mus musculusUnder metabolic stress, the LRRK2-G2019S mutation accelerates astrocytic senescence by physically sequestering DDB1. This aberrant interaction impedes the CUL4–DDB1-mediated proteasomal degradation of p21, leading to massive p21 accumulation, an exacerbated senescence-associated secretory phenotype (SASP), and subsequent neurodegeneration. Crucially, non-invasive LED-PBM dismantles this pathogenic axis by selectively disrupting the LRRK2–DDB1 interaction, thereby restoring p21 clearance and uncoupling metabolic dysfunction from neuronal injury.Transcriptomic profiling via microarray was employed to unbiasedly interrogate global gene network alterations driven by the interaction between metabolic stress and the LRRK2-G2019S mutation
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9. GSE303576 Rb驱动的转录限制了其在乳腺癌中的肿瘤抑制作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensThis SuperSeries is composed of the SubSeries listed below.
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详细内容（全部1条）

1. 新型维生素B12疗法有望对抗致命脑癌

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers have identified a vitamin B12–based compound that can cross the blood-brain barrier and home in on glioblastoma tumors. In animal studies, the compound accumulated preferentially in tumor tissue and delivered sustained nitric oxide directly to cancer cells. It also worked synergistically with existing glioblastoma treatments, significantly enhancing their tumor-fighting effects.
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