详细内容（全部5条）

1. ⭐ GSE253330 肠脑轴调节肝脏抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Bauer Kylynda ; Trehan Rajiv ; Ma Chi ; Greten TimSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHepatic immunosuppression contributes to high mortality in liver cancer. Nerve activity has been implicated in peripheral immune response and tumor growth. Whether cholinergic neuroimmune interactions shape hepatocellular carcinoma (HCC) remains uncertain. Hepatic vagotomy significantly reduced primary and metastatic liver tumors in mice. These vagotomized livers exhibited anti-tumor immunity, notably elevated inflammatory and cytotoxic CD8+ T cell subsets. Pharmaceutical or genetic disruption of ACh activity regulated CD8+ T cell function via AChR Chrm3, while tumor growth was rescued in Rag1KO mice or following CD8+ T cell depletion. Beyond tumor-specific outcomes, vagotomy improved cancer-associated fatigue and anxiety-like behavior. As microbiota transplantation from HCC donors was sufficient to impair behavior, we performed microbiome sequencing throughout cohousing and microbiota transplantation studies. Tumor, rather than vagotomy, robustly altered fecal bacterial composition, increasing Desulfovibrionales and Clostridial taxa. This tumor microbiota was sufficient to promote anti-tumor CD8+ T cell immune features only within vagotomized, but not vagal-intact, tumor-free mice. We identify gut-brain ACh signaling as a critical, dynamic, and targetable arc to modulate liver immunity and cancer outcomes.
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2. ⭐ GSE315767 人类结直肠癌细胞系ECM1敲低后的转录组测序分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、sequencing、transcriptome
• 📝 描述：Contributor : Huihui XiaoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo investigate the regulatory role of ECM1 in CCL20 expression in colorectal cancer, this study employed the human colorectal cancer SW620 cell line. Stable knockdown of ECM1 gene expression was achieved via shRNA, and single-cell transcriptome sequencing technology was used to systematically compare the transcriptomic differences between the ECM1 knockdown group (SW620-shECM1) and the negative control group (SW620-shNC). Sequencing analysis revealed that ECM1 knockdown significantly affected multiple signaling pathways, among which the TNF-α signaling pathway was notably activated, and the expression and activity of the key transcription factor JUNB underwent significant changes. Further mechanistic studies demonstrated that ECM1 regulates the transcription and expression of the downstream chemokine CCL20 by modulating the TNF-α/JUNB signaling axis. This study is the first to reveal the molecular mechanism by which ECM1 regulates CCL20 through the TNF-α-JUNB pathway in colorectal cancer at the single-cell level, providing a new perspective for understanding the role of ECM1 in the tumor microenvironment and immune regulation.
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3. GSE299736 刚度感知驱动基质代谢重启，促进肾脏修复和再生 [Visium]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、Visium
• 📝 描述：Contributors : Yuan Gui ; Yuanyuan Wang ; Wenxue Li ; Jia-Jun Liu ; Kelly Zheng ; Jianzhong Li ; Henry Wells Shaffer ; Cameron Jones ; Samantha Mae Mallari ; Yanbao Yu ; Silvia Liu ; Yansheng Liu ; Dong ZhouSeries Type : OtherOrganism : Mus musculusKidney repair after acute kidney injury (AKI) relies on a finely tuned extracellular matrix (ECM) that provides both structural integrity and mechanical cues. As primary ECM architects, fibroblasts and pericytes rapidly mobilize to the injury site post-AKI, yet the ECM-driven repair mechanisms remain inadequately understood. Leveraging data-independent acquisition-based proteomics, spatial transcriptomics, genetic and pharmaceutical models, and tissue engineering, we profiled the proteome landscape of decellularized kidney matrix scaffold post-AKI and highlighted microfibrillar-associated protein 2 (Mfap2) as a key core matrisome component. Sourced primarily from fibroblasts and pericytes, Mfap2 loss disrupts kidney architecture and metabolic balance, aggravating AKI. Global proteomics revealed that Mfap2 knockout downregulates tubule-derived 3-hydroxy-3-methylglutaryl-CoA synthase 2 (Hmgcs2) via estrogen receptor 2 (Esr2)-mediated transcriptional repression and elevated post-translational succinylation. Phosphoproteomics further uncovered a shift in mechanical signaling, where Mfap2 deficiency hyperactivates mitogen-activated protein kinases, driving large tumor suppressor kinase 1 (Lats1) in tubular cells without altering integrin receptor activity. Mechanistically, Lats1 suppression amplifies Esr2 transcription without affecting its ubiquitin-mediated degradation, functioning independently of the canonical Yap/Taz signaling. Remarkably, Esr2 agonists restored kidney function in Mfap2-deficient models. These findings position Mfap2 as a key regulator of ECM stiffness and mechanical signaling, orchestrating metabolic reprogramming and a pro-repair microenvironment essential for kidney repair and regeneration.
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4. GSE311755 HCQ 治疗小鼠肺细胞的单细胞基因表达谱。

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：Contributors : Hideo Negishi ; Yusuke Wada ; Tatsuma Ban ; Ken J IshiiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe performed single-cell RNA sequencing (scRNA-seq) of lung cells from hydroxychloroquine (HCQ)-treated mice to examine HCQ-induced IFN-I response in the lung.
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5. GSE311546 用 HCQ 或 cGAMP 处理的 GM-CSF 培养的骨髓细胞的单细胞基因表达谱。

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：Contributors : Hideo Negishi ; Yusuke Wada ; Tatsuma Ban ; Ken J IshiiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe performed single-cell RNA sequencing (scRNA-seq) of granulocyte-macrophage colony-stimulating factor (GM-CSF) cultured bone marrow cells (GM-BMCs) treated with hydroxychloroquine (HCQ) or cyclic guanosine monophosphate–adenosine monophosphate (cGAMP) to reveal a divergence of the gene expression pattern in interferon β (IFNβ)-expressing cells between HCQ and cGAMP treatments.
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详细内容（全部1条）

1. ⭐ 科学家发现肠道中一个隐藏的衰老程序，该程序会增加患癌风险。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、aging、gut、regex:gut(-?microbiome)?
• 📝 描述：Although the gut renews itself constantly, its stem cells accumulate age-related molecular changes that quietly alter how genes are switched on and off. Scientists found that this “epigenetic drift” follows a clear pattern and appears in both aging intestines and most colon cancers. Some regions age faster than others, forming a patchwork of weakened tissue more prone to degeneration. Encouragingly, researchers showed this drift can be slowed—and partly reversed—by restoring iron levels or key cellular signals.
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