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1. ⭐ GSE318119 铁凋亡肿瘤细胞重塑肿瘤相关巨噬细胞抗原呈递，从而释放免疫检查点阻断疗法的疗效

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、macrophage、antigen
• 📝 描述：Contributors : Jia lei Sun ; Dingdang Yu ; Shibin Hu ; Jimin ZhuSeries Type : Genome binding/occupancy profiling by high throughput sequencing ; Other ; Expression profiling by high throughput sequencingOrganism : Mus musculusActivation of antigen presentation has been shown to contribute to improved immunotherapy outcomes. Herein, we show that inducing tumor cell ferroptosis boosts anti-tumor immunity by potentiating major histocompatibility complex II (MHC-II)- dependent antigen presentation in tumor-infiltrating macrophages. Supporting our findings with multi-omics data, we reported that ferroptotic tumor-derived all-trans retinoic acid (ATRA) is a novel regulator of MHC-II in macrophages. ATRA directly targets CD38 through transcriptional factor RARα and activates master regulator TFEB to control MHC-II expression by inducing autophagy. Clinically, a ferroptosis signature is associated with better immunotherapy response. We also innovatively develop a drug-free nano-redox lever (DFNRL) to circumvent the non-specific limitations of conventional drugs, which specifically targets and disrupts glutathione metabolism in tumor cells by accepting electrons, thereby boosting ferroptosis-mediated immune stimulation. This synergizes with anti–PD-1 immunotherapy across preclinical models. Our study answers an unidentified role for ferroptosis in modulating anti-tumor immunity and provides a clinically translatable approach to enhance immunotherapy efficacy.
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2. GSE306753 Z-RNA 驱动 Tau 介导的阿尔茨海默病神经退行性变 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、RNA-seq
• 📝 描述：Contributor : Boxin ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTau aggregates lead to progressive neurodegeneration in Alzheimer’s disease (AD) (ref). Neuron death is one of the hallmarks of neurodegeneration (ref). However, the pathological influence of neuronal death is undetermined, and the connection between Tau aggregates and neuronal death remains elusive. Here we demonstrated the essential role of neuron death in Tau-related neurodegeneration. Tau-neurons died in necroptosis, dependent on ZBP1 sensitized by Z-RNAs (an unusual left-handed conformation). Those endogenous Z-RNAs were transcripts of reactivated transposable elements (TEs) originally silenced in heterochromatin.
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3. GSE306751 Z-RNA 驱动 Tau 介导的阿尔茨海默病神经退行性变 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、ChIP-seq
• 📝 描述：Contributor : Boxin ZhangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTau aggregates lead to progressive neurodegeneration in Alzheimer’s disease (AD). Neuron death is one of the hallmarks of neurodegeneration. However, the pathological influence of neuronal death is undetermined, and the connection between Tau aggregates and neuronal death remains elusive. Here we demonstrated the essential role of neuron death in Tau-related neurodegeneration. Tau-neurons died in necroptosis, dependent on ZBP1 sensitized by Z-RNAs (an unusual left-handed conformation). Those endogenous Z-RNAs were transcripts of reactivated transposable elements (TEs) originally silenced in heterochromatin.
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4. GSE324468 靶向 E 蛋白可增强 cDC1 的免疫原性，从而实现强效抗肿瘤疫苗接种 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、ChIP-seq
• 📝 描述：Contributors : Xiaoyu Zhai ; Ping Gao ; Xiaojuan Han ; Xi Wang ; Xiangwen Liu ; Chao Li ; Yuanyuan Shi ; Baidong Hou ; Xuyu Zhou ; Jianwei Wang ; Jian Song ; Fuping ZhangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusType 1 conventional dendritic cells (cDC1s) are essential for priming anti-tumor CD8⁺ T cells, yet the intrinsic pathways limiting their function remain unclear. Here we identify E-proteins (E2A/HEB) as a master checkpoint that actively suppresses cDC1 immunogenicity by directly transactivating PTEN, thereby restraining PI3K-AKT-mTOR signaling, FLT3L-driven proliferation, and NF-κB-mediated IL-12 production. Genetic ablation of E-proteins in DCs unleashes a hyperfunctional program—expanded cDC1 populations, enhanced antigen presentation, and superior CD8⁺ T cell priming—while deletion of the E-protein antagonist Id2 impairs cDC1 function, establishing a bidirectional rheostat. This axis is clinically relevant, as dynamic E-protein activity in human tumor DCs correlates with patient survival and response to immune checkpoint blockade. Finally, vaccination with E-protein-deficient DCs elicits potent antigen-specific T cell expansion and achieves robust therapeutic efficacy across multiple preclinical tumor models, defining a targetable checkpoint and establishing E-protein inactivation as a platform for next-generation cancer immunotherapies.
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5. GSE324467 靶向 E 蛋白可增强 cDC1 的免疫原性，从而实现强效抗肿瘤疫苗接种 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、RNA-seq
• 📝 描述：Contributors : Xiaoyu Zhai ; Ping Gao ; Xiaojuan Han ; Xi Wang ; Xiangwen Liu ; Chao Li ; Yuanyuan Shi ; Baidong Hou ; Xuyu Zhou ; Jianwei Wang ; Jian Song ; Fuping ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusType 1 conventional dendritic cells (cDC1s) are essential for priming anti-tumor CD8⁺ T cells, yet the intrinsic pathways limiting their function remain unclear. Here we identify E-proteins (E2A/HEB) as a master checkpoint that actively suppresses cDC1 immunogenicity by directly transactivating PTEN, thereby restraining PI3K-AKT-mTOR signaling, FLT3L-driven proliferation, and NF-κB-mediated IL-12 production. Genetic ablation of E-proteins in DCs unleashes a hyperfunctional program—expanded cDC1 populations, enhanced antigen presentation, and superior CD8⁺ T cell priming—while deletion of the E-protein antagonist Id2 impairs cDC1 function, establishing a bidirectional rheostat. This axis is clinically relevant, as dynamic E-protein activity in human tumor DCs correlates with patient survival and response to immune checkpoint blockade. Finally, vaccination with E-protein-deficient DCs elicits potent antigen-specific T cell expansion and achieves robust therapeutic efficacy across multiple preclinical tumor models, defining a targetable checkpoint and establishing E-protein inactivation as a platform for next-generation cancer immunotherapies.
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6. GSE322653 cFLIP的表达是弥漫性大B细胞淋巴瘤发病机制所必需的

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymphoma、B cell
• 📝 描述：Contributors : Kristie Bariboloka ; Justinas Valiulis ; Martin Peifer ; Alessandro AnnibaldiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDiffuse large B cell lymphoma (DLBCL) is a highly heterogenous malignant disease that remains a major clinical challenge as relapsed and refractory disease is difficult to treat. Apoptosis evasion is a major feature of DLBCL. However, while the suppression of intrinsic apoptosis has long been recognized as a lymphoma-promoting event, the role of extrinsic apoptosis has remained poorly defined. Here, we demonstrated at the genetic level that expression of cFLIP, the most crucial, non-redundant inhibitor of extrinsic apoptosis, in B cells is necessary for the development of diffuse large B cell lymphoma (DLBCL) in an autochthonous murine model. Indeed, B cell-specific deletion of Cflar, the gene encoding for cFLIP, prevented lymphomagenesis mediated by oncogenic Myd88 and overexpression of BCL2. In human lymphoma cells, we showed that the absence of cFLIP sensitizes ABC- but not GCB DLBCL subtype cells to TRAIL- or LPS-induced, Caspase-8-mediated apoptosis. Furthermore, we unveiled a cell death-independent role of cFLIP in the suppression of pro-inflammatory cytokines at the transcriptional level, selectively in the ABC subtype. These results indicate that the suppression of intrinsic apoptosis can support lymphomagenesis only if extrinsic apoptosis is properly controlled. Moreover, licensing extrinsic apoptosis via cFLIP deletion can efficiently promote the death of DLBCL cells despite the suppression of the intrinsic pathway. Overall, these data provide the rationale for the development of cFLIP inhibitors for the treatment of ABC DLBCL and possibly other haematological cancers.
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7. GSE292480 m5C 协调因子 NSUN7 驱动 SPARC/HMGB1 轴介导的炎症，从而加剧肾损伤 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、RNA-seq
• 📝 描述：Contributors : Yuhang Dong ; Xiaoming MengSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensGrowing evidence indicates that kidney inflammation is a major contributor to the pathogenesis of various renal diseases, including acute kidney injury (AKI). Although RNA modifications have been implicated in regulating kidney inflammation, their precise roles remain largely unknown. Here, we show that kidney inflammation and injury were associated with elevated RNA 5-methylcytosine (m5C) modifications, primarily driven by the m5C “writer” NOP2/Sun RNA methyltransferase family member 7 (NSUN7). Both global and kidney-specific deletion of Nsun7 in mice reduced m5C abundance, attenuated inflammatory responses, and decreased macrophage infiltration, underscoring its proinflammatory role in the kidney. Mechanistically, we identified secreted protein acidic and cysteine-rich (SPARC) as a major downstream effector of NSUN7. SPARC upregulation amplified inflammatory responses in renal tubular epithelial cells by interacting with high mobility group box 1 and further promoted proinflammatory macrophage infiltration via tubular-macrophage crosstalk. Notably, therapeutic silencing of Nsun7 using a kidney-specific DNA tetrahedral molecular carrier developed for this study effectively alleviated inflammation and improved renal outcomes in AKI models. Collectively, our findings identify NSUN7 as a key driver of renal inflammation via SPARC regulation and underscore its potential as a therapeutic target in inflammatory kidney diseases.
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8. GSE292184 FOXM1驱动结直肠癌脑转移的代谢适应，并代表一个潜在的治疗靶点

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolic
• 📝 描述：Contributors : Fayhaa Khair-Dabour ; Inbal Greenberg ; Sivan Fuchs ; Guy Shapira ; Asia Zubkov ; Ido Wolf ; Tami RubinekSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensColorectal cancer (CRC) is a leading cause of cancer-related mortality in the Western world. While brain metastasis (BMs) are relatively uncommon in CRC, they represent the fourth most frequent cause of BMs overall and their occurrence is increasingly recognized as a complication in advanced CRC, associated with poor prognosis and limited treatment options. The brain microenvironment presents unique metabolic challenges, including low oxygen levels and restricted lipid availability. In order to survive in this hostile environment, CRC cells must acquire metabolic adaptations allowing them to survive and proliferate. To identify key drivers that enable CRC cells to metastasize to and survive within the brain, we conducted a transcriptomic screen of CRC BMs. Among the upregulated genes, FOXM1 was identified, a transcription factor critical for tumor progression. This was further validated by immunohistochemistry in human samples. To study the role of brain microenvironment in mediating FOXM1 upregulation, CRC cells were cultured in either astrocyte-conditioned media (A-CM) or compared to hepatocyte-conditioned media (H-CM). CRC cells exposed to A-CM exhibited markedly higher FOXM1 expression. Moreover, using an in vivo model of intracranial CRC BM mouse model demonstrated significant FOXM1 overexpression in CRC cells following brain injection. And notably, our study revealed a significant correlation between FOXM1 and fatty acid synthase (FASN) in the brain microenvironment. These findings suggest that FOXM1 plays a key role in CRC brain metastasis and may serve as a promising therapeutic target. Targeting FOXM1 could provide novel treatment strategies for CRC patients with BMs, potentially improving outcomes in this challenging disease setting.
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9. GSE261853 SMYD3 通过 SREBP1 介导的 CD47 转录激活促进透明细胞肾细胞癌的免疫逃逸

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、immune
• 📝 描述：Contributors : Zhengfang Liu ; Xiumei Zhao ; Bo Han ; Shouzhen ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe field of immunotherapy for clear cell renal cell carcinoma (ccRCC) is rapidly expanding over the past decade, but limited success to date. Cancer cell-intrinsic features (e.g., genetic aberrations, dysregulation of signaling pathway) play a pivotal role in orchestrating the composition and functional state of immune landscape, which in turn impact tumor progression and response to immunotherapy. However, the underlying mechanism of crosstalk between renal cancer cell and immune cell is largely unknown. Here we discovered that cancer cell-intrinsic SET and MYND domain-containing protein 3 (SMYD3) dysregulation orchestrated an immunosuppressive microenvironment and impaired responses to PD-1 blockade by reprograming the infiltration of immune cells in tumor microenvironment (TME) of ccRCC. Mechanistically, SMYD3, a chromatin regulator, cooperated with Sp1 to transcriptionally promote sterol regulatory element-binding protein 1 (SREBP1) expression by modifying H3-K4 di-/trimethylation and consequently activating the transcription of CD47. CD47, a bridge between innate and adaptive immunity, acted as the downstream effector molecule of the SMYD3 signal to promote the infiltration of Th2 cells, protecting renal cancer cell from immune attack. In summary, we elucidated a critical role for cancer cell-intrinsic SMYD3-SREBP1-CD47 signal in the regulation of the immune microenvironment in ccRCC, and provided a potential strategy to manipulate the tumor immune milieu in favor of antitumor immunity.
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10. GSE318076 AURKA抑制剂VIC-1911诱导有丝分裂缺陷和功能性BRAC，使前列腺癌对PARP抑制剂敏感

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributors : Galina Gritsina ; Qi Chu ; Jonathan C Zhao ; Jindan YuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensVIC-1911, formerly known as TAS-119, is a next-generation, ATP-competitive AURKA inhibitor with high selectivity over AURKB and AURKC. In this study, we demonstrate that VIC-1911 potently and selectively inhibits AURKA signaling in diverse prostate cancer (PC) cell models, including both androgen receptor (AR)-positive and AR-negative cell lines. VIC-1911 treatment suppressed AURKA phosphorylation and downstream effectors at nanomolar concentrations without affecting AURKB/C activity, resulting in mitotic defects, DNA double-strand breaks (DSBs), and apoptosis. Transcriptomic profiling and immunofluorescence analysis revealed robust activation of DNA damage response pathways and the p53 pathway, consistent with mitotic catastrophe-induced genotoxic stress. Functionally, VIC-1911 significantly inhibited PC cell proliferation and tumor growth in xenograft models, including castration-resistant and AR-negative tumors. Given its ability to induce DNA damage, we evaluated the combinatorial effect of VIC-1911 with PARP inhibitors (PARPi). The combination exhibited synergistic anti-tumor effects in vitro and in vivo, leading to enhanced mitotic abnormalities, γH2AX accumulation, and cleaved PARP expression, even in homologous recombination (HR)-proficient settings. Importantly, VIC-1911 monotherapy and its combination with PARPi were well tolerated in vivo. These findings position VIC-1911 as a promising therapeutic agent for advanced prostate cancer, either as monotherapy or in combination with PARPi to broaden clinical efficacy beyond HR-deficient tumors
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1. 父亲吸烟与子女代谢变化有关

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic
• 📝 描述：A new study in mice suggests that a father’s nicotine exposure could influence the metabolic health of his children. Researchers found that when male mice consumed nicotine, their offspring showed changes in how their bodies handled sugar, including differences in insulin and glucose levels and altered liver function. These shifts may be linked to a higher risk of diabetes and related metabolic diseases.
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2. 科学家发现ALS蛋白将DNA修复与癌症和痴呆症联系起来

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A protein tied to ALS and dementia may have a much bigger role in disease than scientists realized. Researchers found that TDP43 controls a key DNA repair process, but when the protein becomes imbalanced, the repair system can spiral out of control, harming neurons and destabilizing DNA. The team also discovered that high levels of the protein are linked to increased mutation rates in cancer. The discovery places TDP43 at the center of both neurodegeneration and cancer biology.
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3. 甜甜圈状蛋白质分解，启动细菌细胞分裂。

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:bacter(ia|ial|ium)
• 📝 描述：Researchers have revealed how bacteria precisely control the genes that trigger cell division. The study shows that the MraZ protein, which normally forms a donut-shaped structure, must bend and partially break apart to bind key DNA sequences that activate division genes. Using cryo-electron microscopy, scientists captured this interaction in remarkable detail. The mechanism appears to be widespread across bacteria, offering a new window into how microbes regulate growth.
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• GSE306761 Z-RNA 驱动 Tau 介导的阿尔茨海默病神经退行性变 [bulkRNA-seq]
• GSE306739 Z-RNA驱动Tau介导的阿尔茨海默病神经退行性变
• GSE266668 小鼠 DNA 甲基化模式的非孟德尔遗传广泛存在。
• GSE324442 全球生态系统服务昆虫——果酱食蚜蝇 Episyrphus balteatus 的全面阶段和组织特异性转录组
• GSE324138 子宫肌瘤及其匹配的子宫肌层中非编码RNA启动子甲基化状态的比较分析
• GSE323991 解读PURA综合征：PURA缺失会改变神经细胞命运决定并损害神经元稳态
• GSE315227 RNA-seq 数据，比较 PEPD 过表达与 NC GBM 细胞
• GSE313946 数学模型揭示了耐药癌细胞持续存在细胞中由核糖体水平诱导的存活检查点
• GSE311942：在UVA1照射下，转染tRF-34模拟物或阴性对照的人真皮成纤维细胞的转录组分析
• GSE308216 一种生物混合手性水凝胶通过多管齐下抑制肿瘤干性来增强临床前术后胶质母细胞瘤治疗效果
• GSE293257 TGF-β1抑制IL-1β诱导的人滑膜成纤维细胞趋化因子表达
• GSE292304 m5C 协调者 NSUN7 驱动 SPARC/HMGB1 轴介导的炎症，从而加剧肾损伤 [MeRIP-Seq]
• GSE292038 CITE-Seq 分析了接受抗 PD-1 疗法治疗的 YUMM1.7 黑色素瘤的肿瘤内免疫细胞。
• GSE261616 SS-31 通过抑制 MAPK 信号通路来保护肺部免受百草枯引起的损伤和纤维化。