科研日报 2026-01-02

Page content

📅 Daily Report - 2026-01-02

今日筛选出 191 条内容,来自 2 个来源

Powered by 科研普拉斯 & Claude

🤖 今日AI智能总结

🧬 数据前沿

今日焦点

  1. 新型细菌疗法:研究发现,将章鱼启发的三重工程菌用于癌症免疫治疗,有望克服现有细菌疗法的精准度和安全性挑战。
  2. 肿瘤微环境与免疫逃逸:揭示了胞内细菌促进乳腺癌复发中的免疫逃逸机制,以及缺氧诱导的HIF-1α乳酸化在食管鳞状细胞癌免疫逃逸中的关键作用。

主要方向

  • 肿瘤免疫微环境调控:探索胞内细菌、TREM2+巨噬细胞、TGF-βRII/IL-15复合物、METTL3介导的m6A修饰以及缺氧对肿瘤免疫逃逸的影响。
  • 癌症治疗策略开发:包括章鱼启发工程菌、CAR-T细胞疗法、以及靶向CD8+ T细胞的免疫复合物。
  • 细胞衰老与免疫:研究NRF1介导的先天免疫响应在细胞衰老和老化中的作用。

技术亮点

  • 单细胞多组学结合:CBTi-seq技术实现了小鼠大脑功能区域的空间分辨单细胞转录组学分析。
  • ATAC-seq与RNA-seq联合应用:用于解析乳腺癌转移中TREM2+巨噬细胞的作用,以及食管癌中HIF-1α乳酸化和METTL3介导的m6A修饰。

🧪 博客更新

今日焦点: 两项最新研究揭示了衰老和癌症风险的新机制:免疫系统衰退与高脂饮食驱动肝癌。

主要方向

  • 探究血小板因子4(Platelet Factor 4)蛋白水平下降如何加速免疫系统衰老。
  • 评估高脂饮食对肝脏细胞生存模式的影响及其与肝癌早期风险的关联。

技术亮点

  • 识别出关键蛋白在免疫衰老中的作用。
  • 揭示了高脂饮食诱导肝细胞进入特定生存模式的新机制。

📚 分类浏览

🧬 数据前沿 (189条)

详细内容(前10条)

1.GSE275604 肿瘤细胞胞质细菌促进乳腺癌转移复发期间的免疫逃逸

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、cancer、immune、bacteria、regex:bacter(ia|ial|ium)
  • 📝 描述:Contributors : Bingqing Yao ; Xiaoqin Liu ; Xiunan Fang ; Yajing Guo ; Shang CaiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIntratumor microbiota represents an understudied yet influential component of the cancer ecosystem, impacting the physical, chemical and immunological tumor microenvironment. However, the interplay between intratumor microbiota and the tumor-immune network as well as its physiological significance remain poorly understood. In this study, we investigated the long-term developmental process of metastatic seeds from PyMT breast tumor, and identified the key role of intratumor bacteria for efficient metastasis outgrowth after tumor cell colonization in distant organ in an immune-mediated process. Cytosolic bacteria, the dominant form of intratumor bacteria in PyMT tumors, promote metastatic tumor cell immune evasion through activating tumor cell intrinsic cGAS-STING-Il17b response pathway, ultimately inducing neutrophil into a protumor state to suppress cytotoxic T cells. Intriguingly, the upregulation of Il17b is dependent on the intracellular invasion of bacteria and accumulation of cytosolic dsDNA. The extracellular bacteria can not activate the STING pathway but induce neutrophils into an anti-tumor state instead. Under the physiological condition, the eradication of intracellular bacteria effectively abrogates metastatic immune suppression and prevents post-surgical metastatic recurrence, akin to the effect of introducing extracellular bacteria. Our findings underscore the critical role of intratumor bacteria in modulating the immune landscape of recurrent metastatic niches, and emphasize the bacteria-host interaction mode as a novel key factor for immune regulation.
  • 🔗 查看原文

2.GSE250146 Octopus-inspired triple-engineered bacteria for precision cancer immunotherapy

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、bacteria、regex:bacter(ia|ial|ium)、regex:immuno(logy|therapy|suppression)
  • 📝 描述:Contributors : Leyang Wu ; Lin Li ; Zichun HuaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBacterial cancer therapies face precision and safety challenges, which limit their clinical application. This study presents a triple-engineered Salmonella typhimurium strain (OITE-bacteria), designed for targeted cancer therapy, inspired by octopus biology and leveraging synthetic biology and biomimetic principles. The strain incorporates SpyTag proteins on the outer membrane, allowing covalent attachment of SpyCatcher-fused quadruple RGD peptides to enhance tumor adhesion via integrin αvβ3 interactions. This promotes bacterial enrichment in various solid tumors and lung metastases. Subsequently, Quorum sensing induces expression of strain HtrA protein within tumors, enhancing extracellular polysaccharide-mediated immunogenicity for activating immune cells. Additionally, the bacteria locally release anti-PD1 nanobodies to anti-immunosuppressive. In murine models, OITE-bacteria achieved a ninefold increase in tumor colonization within 12 hours and sustained melanoma growth suppression for over 40 days, with a 100% response rate. This modular approach, integrating safety and efficacy, provides a new strategy in microbial therapeutics for solid tumors.
  • 🔗 查看原文

3.GSE301873 TGF-βRII/IL-15 免疫治疗复合物靶向淋巴结和肿瘤中耗竭的 CD8+ T 细胞亚群

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:lymph、T cell、regex:lymph(o|atic)?
  • 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusExhausted CD8+ T cells, located within the tumor-draining lymph nodes (TDLNs) are responsible for maintaining tumor-specific responses in cancer. Here, we demonstrate that a bifunctional TGF-βRII/IL-15 protein complex (HCW9218), with TGF-β neutralization and IL-15 immunostimulatory activities, is capable of localizing to the TDLNs and tumors after subcutaneous administration, neutralizes TGF-β, expands progenitor stem-like exhausted T cells (TPEX) in TDLNs, and promotes their infiltration into tumors. Immune-checkpoint-inhibitors (ICIs) significantly enhanced the effects of HCW9218 on TPEX, and synergistically improved HCW9218 anti-tumor efficacy in melanoma and reduced spontaneous lung metastasis in breast cancer models. In a dose-escalating clinical trial in patients with chemo-refractory/relapsed solid tumors, HCW9218 monotherapy was well-tolerated, reduced serum TGF-β levels, promoted CD8+ T cell expansion in peripheral blood and CD8+ T cell infiltration in tumor biopsies. These findings provide a strong basis for using HCW9218 to enhance the efficacy of ICIs against solid tumors in the clinical setting.
  • 🔗 查看原文

4.GSE295918 TREM2+巨噬细胞浸润是紫杉醇治疗引起的乳腺癌肺转移的基础[ATAC-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、macrophage、ATAC-seq
  • 📝 描述:Contributors : Yuqi Xing ; Hongquan Zhang ; Jun ZhanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusMetastasis is a major cause of breast-cancer-related death and frequently occurs following paclitaxel neoadjuvant chemotherapy failure. Tumor microenvironment contributes to metastasis, while the role of specific host cells in lung metastases induced by paclitaxel (PTX) treatment remains poorly understood. Here, we demonstrate that PTX neoadjuvant chemotherapy promotes triggering receptor expressed on myeloid cells-2 (TREM2)-positive macrophage infiltration in the breast cancer tissues of patients. Meanwhile, we also show that more TREM2-positive macrophage infiltrates in breast cancer tissues of patients with lung -metastasized. Genetic TREM2 deficiency decreases breast cancer lung metastases induced by PTX treatment in vivo, suggesting that TREM2-positive macrophages are essential for PTX-promoting lung metastasis of breast cancer. We further reveal that PTX promotes tumor cell secretion of fibroblast growth factor 2 (FGF2), triggering TREM2 transcription via upregulating its transcriptional factor early growth response-1 (EGR1) in macrophages. Increased TREM2 activates epithelial-mesenchymal transition (EMT)-related cytokine secretion in macrophages, inducing tumor cell lung metastases. Targeting TREM2 significantly suppressed lung metastasis in breast-cancer-bearing mice. Our findings establish that tumor-cell-derived FGF2 induced by paclitaxel treatment upregulates TREM2 in myeloid macrophages, which in turn promotes the EMT of neighboring tumor cells through cytokine secretion. Our results highlight TREM2 as a potential therapeutic target to mitigate lung metastasis due to PTX treatment.
  • 🔗 查看原文

5.GSE292981 外周血单核细胞对不同免疫佐剂刺激的单细胞转录组分析

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、single-cell、transcriptome
  • 📝 描述:Contributors : Ken Takashima ; Hiroyuki OshiumiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensImmune adjuvants are agents that enhance the immunogenicity of vaccines when co-administered with antigens. While their primary mode of action involves activation of innate immune pathways in antigen-presenting cells such as myeloid cells—leading to cellular maturation and enhanced antigen presentation—how adjuvants affect other hematopoietic cell types remains largely unclear. To address this, we performed single-cell RNA sequencing of human PBMCs treated with various immune adjuvants, aiming to characterize cell type–specific transcriptional responses at single-cell resolution.
  • 🔗 查看原文

6.GSE315099 HIF-1α 在 K172 位点的乳酸化驱动 HIF1 复合物组装,从而促进食管鳞状细胞癌中缺氧诱导的免疫逃逸 [ATAC-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:carcinoma、immune、ATAC-seq
  • 📝 描述:Contributors : Ji Cong ; Sujuan ZhengSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensHypoxia is a hallmark of the tumor microenvironment, but its role in immune evasion in esophageal squamous cell carcinoma (ESCC) remains to be fully elucidated. Here, we demonstrate hypoxia inversely correlated with anti-tumor immune signatures and CD8+ T cell infiltration in clinical samples and murine models. Functionally, reducing hypoxia with the agents TH-302 or PX-478 in the AKR model enhanced intratumoral CD8+ T cell infiltration and increased their expression of Granzyme B, IFNγ, and TNFα. Mechanistically, hypoxia-induced immune suppression was dependent on protein lactylation. Inhibiting lactylation reversed the hypoxic suppression of CD8+ T cell function and abrogated the hypoxia-driven transcriptional program, which involved pathways like glycolysis, TGFβ, and Notch signaling. This lactylation-dependent regulation operated by facilitating the formation of the HIF1 transcription complex. Specifically, mass spectrometry identified lactylation at the K172 site of HIF1α, which was crucial for its binding to HIF1β and subsequent target gene activation. Furthermore, in a preclinical ESCC model, pharmacological inhibition of HIF1α with PX-478 synergized with anti-PD-1 therapy, leading to superior tumor control and enhanced CD8+ T cell cytotoxicity. Our study identifies HIF1α K172 lactylation as a pivotal mechanism of hypoxia-mediated immune escape in ESCC, suggesting a therapeutic strategy to improve immunotherapy.
  • 🔗 查看原文

7.GSE315097 HIF-1α 在 K172 位点的乳酸化驱动 HIF1 复合物组装,从而促进食管鳞状细胞癌中缺氧诱导的免疫逃逸 [RNA-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:carcinoma、immune、RNA-seq
  • 📝 描述:Contributors : Ji Cong ; Sujuan ZhengSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHypoxia is a hallmark of the tumor microenvironment, but its role in immune evasion in esophageal squamous cell carcinoma (ESCC) remains to be fully elucidated. Here, we demonstrate hypoxia inversely correlated with anti-tumor immune signatures and CD8+ T cell infiltration in clinical samples and murine models. Functionally, reducing hypoxia with the agents TH-302 or PX-478 in the AKR model enhanced intratumoral CD8+ T cell infiltration and increased their expression of Granzyme B, IFNγ, and TNFα. Mechanistically, hypoxia-induced immune suppression was dependent on protein lactylation. Inhibiting lactylation reversed the hypoxic suppression of CD8+ T cell function and abrogated the hypoxia-driven transcriptional program, which involved pathways like glycolysis, TGFβ, and Notch signaling. This lactylation-dependent regulation operated by facilitating the formation of the HIF1 transcription complex. Specifically, mass spectrometry identified lactylation at the K172 site of HIF1α, which was crucial for its binding to HIF1β and subsequent target gene activation. Furthermore, in a preclinical ESCC model, pharmacological inhibition of HIF1α with PX-478 synergized with anti-PD-1 therapy, leading to superior tumor control and enhanced CD8+ T cell cytotoxicity. Our study identifies HIF1α K172 lactylation as a pivotal mechanism of hypoxia-mediated immune escape in ESCC, suggesting a therapeutic strategy to improve immunotherapy.
  • 🔗 查看原文

8.GSE304090 药理学抑制表观遗传酶 EZH2 可减轻心肌梗死小鼠模型中的心脏功能障碍并缓解脂质代谢紊乱

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:metabolism、cardiac、epigenetic
  • 📝 描述:Contributors : Sylvain Fraineau ; Hugues Boël ; Matthieu RuizSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusRational: EZH2, an epigenetic enzyme, acts as a transcriptional repressor for genes dysregulated after myocardial infarction (MI). Objective: This study aims to assess the benefits of GSK-343 (EZH2 inhibitor) on cardiac function and lipid metabolism after MI. Methods: Mice were treated daily with vehicle or GSK-343 for 7 days after MI and we evaluated cardiac function (echocardiography), gene expression profiling (RNA-seq) and circulating lipidome (untargeted lipidomics). Results: The 28% MI decreased ejection fraction (EF) was improved by 20% with GSK-343. RNA-seq analysis revealed wide changes in MI normalized with GSK-343: 16 mitochondrial DNA-encoded genes, 57 genes related to mitochondrial function and 15 to lipid metabolism among the 561 down-regulated genes (FC 0.5 and 2; p=10-4). In plasma, while MI enhanced 18 triglycerides (1.24-2.43-fold; p<0.05) and decreased 32 choline glycerophospholipids (PC; 0.55-0.81-fold, p<0.05), GSK-343 normalized these perturbations. In MI, some of these lipids positively correlated with EF (e.g. PC40:6; R=0.84, p=0.004) or with cardiac hypertrophy (e.g. DG18:1_18:2; R=0.81, p=0.007) and GSK-343 abolished most of these correlations. Conclusion: Our study suggests that inhibiting EZH2 is of therapeutic interest to normalize lipid metabolism perturbations and improve cardiac function after MI.
  • 🔗 查看原文

9.GSE304005 CBTi-seq 分析小鼠脑功能区的空间分辨单细胞转录组学

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:single-cell、spatially、transcriptomics
  • 📝 描述:Contributors : Liyong He ; Kaitong DangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo evaluate the potential utility of the CBTi-seq for spatially resolved transcriptomics tissue analysis, we performed a proof-of-concept experiment by microneedle sampling and analyzing three typical mouse brain regions (cerebral cortex (Ccx), corpus callosum (Cc), and hippocampus (Hi)) under the specific zone. CBTi-seq enables spatially resolved transcriptomics analysis in the tissue microenvironment, and holds great potential for revealing the spatial and temporal characteristics and functional heterogeneity of cells.
  • 🔗 查看原文

10.GSE303385 基于纳米抗体的 MSLN.CAR-T 细胞疗法在转移性实体瘤中的抗肿瘤作用的时间映射[总 RNA-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、T cell、RNA-seq
  • 📝 描述:Contributors : Chaido Stathopoulou ; Mingming Zhao ; Qun Jiang ; Jessica Hong ; Jing Bian ; Jingli Zhang ; Mitchell Ho ; Raffit HassanSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusStudies on the dynamic changes occurring in the tumor microenvironment (TME) following CAR-T cell therapy have been confounded by host lymphodepletion, multiple dosing and immunodeficient models. Here, a nanobody-based, mouse mesothelin-targeting CAR-T cell (A101) was developed, achieving effective primary tumor suppression, metastasis reduction, and improved survival after a single dose in immunocompetent, syngeneic mouse models without lymphodepletion. Temporal tumor profiling using RNA sequencing revealed initial downregulation of cell proliferation genes followed by upregulation of inflammation, epithelial-to-mesenchymal-transition (EMT) and extracellular matrix (ECM) modification genes in the CAR-T-treated tumors relative to mock-T-treated controls. This phenotype was reversed at a later timepoint which coincided with downregulation of immunosuppressive Cd274+ Lcn2+ neutrophils and upregulation of anti-tumor P2rx1+ Nrf2- neutrophils. At the same time, upregulation of Ccl2+ in fibroblasts and a more immunomodulatory macrophage phenotype was observed in CAR-T-treated tumors, indicating a tumor adaptation mechanism. This study demonstrates complex dynamic changes in the TME, and highlights time-dependent responses of solid tumors to CAR-T cell therapy. It further highlights Lcn2+ neutrophils and Ccl2+ fibroblasts as potential therapeutic targets for improving CAR-T cell anti-tumor efficacy for solid tumors.
  • 🔗 查看原文

💡 该来源还有 179 条内容,详见 文末

🧪 博客更新 (2条)

详细内容(全部2条)

1. 蛋白质缺失可能导致免疫系统衰老

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、aging
  • 📝 描述:As we age, our immune system quietly loses its edge, and scientists have uncovered a surprising reason why. A protein called platelet factor 4 naturally declines over time, allowing blood stem cells to multiply too freely and drift toward unhealthy, mutation-prone behavior linked to cancer, inflammation, and heart disease. Researchers found that restoring this protein in older mice — and even in human stem cells in the lab — made aging blood and immune cells behave strikingly younger again.
  • 🔗 查看原文

2. 麻省理工学院的研究表明,高脂肪饮食会使肝癌的发生发展获得危险的先机。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:A high-fat diet does more than overload the liver with fat. New research from MIT shows that prolonged exposure to fatty foods can push liver cells into a survival mode that quietly raises the risk of cancer. Faced with ongoing metabolic stress, these cells abandon their normal roles and revert to a more primitive state that helps them endure harsh conditions. Over time, that shift leaves the liver less functional and far more vulnerable to tumor formation, helping explain why fatty liver disease so often precedes liver cancer.
  • 🔗 查看原文

📊 关键词统计

关键词出现次数
cancer32
RNA-seq25
epigenetic17
immune16
single-cell14
sequencing11
ATAC-seq10
transcriptome10
leukemia9
tumor9
aging8
metabolic7
scRNA7
carcinoma6
macrophage6
genome6
pathway5
Neuronal5
antibody5
transcriptomics4

📎 更多内容

🧬 数据前沿 其他内容 (179条)

📅 报告生成时间:2026-01-01 21:38
🤖 由 GitHub Actions 自动生成