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1. ⭐ GSE333904 KRAS 突变重编程 RNA m6A 修饰以驱动结直肠癌中 CD73 依赖性免疫逃逸 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、RNA-seq、KRAS
• 📝 描述：Contributors : Seungjae Shin ; Seung-Pyo Hong ; Jong-Il Kim ; Sung-Yup ChoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusKRAS mutations, present in about 40% of colorectal cancers (CRCs), are strongly associated with an immunosuppressive tumor microenvironment characterized by restricted immune infiltration and poor responses to immunotherapy. Here, we show that KRAS mutations remodel the m6A epitranscriptome to promote immune evasion. Methylated RNA-immunoprecipitation sequencing of isogenic CRC cells revealed that KRAS-mutant cells exhibit increased N6-methyladenosine (m6A) deposition on CD73 mRNAs, enhancing the stability of the transcripts by promoting interaction with IGF2BP3. This m6A modification was driven by TEAD4-dependent recruitment of the METTL3 methyltransferase complex, identifying TEAD4 as a spatial regulator of m6A deposition. Functionally, METTL3 knockdown in KRAS-mutant syngeneic tumors suppressed tumor growth and restored antitumor immunity by increasing CD8⁺ T-cell and natural killer (NK)–cell infiltration in a CD73-dependent manner. Moreover, METTL3 inhibition synergized with anti-PD-1 therapy and a CD73 inhibitor to reduce tumor burden. Together, these findings demonstrate that KRAS-driven m6A remodeling is a key mechanism of immune suppression in CRC and highlight METTL3 as a promising therapeutic target.
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2. ⭐ GSE311797 KRAS 突变重编程 RNA m6A 修饰以驱动结直肠癌中 CD73 依赖性免疫逃逸 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、ChIP-seq、KRAS
• 📝 描述：Contributors : Seungjae Shin ; Seung-Pyo Hong ; Jong-Il Kim ; Sung-Yup ChoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensKRAS mutations, present in about 40% of colorectal cancers (CRCs), are strongly associated with an immunosuppressive tumor microenvironment characterized by restricted immune infiltration and poor responses to immunotherapy. Here, we show that KRAS mutations remodel the m6A epitranscriptome to promote immune evasion. Methylated RNA-immunoprecipitation sequencing of isogenic CRC cells revealed that KRAS-mutant cells exhibit increased N6-methyladenosine (m6A) deposition on CD73 mRNAs, enhancing the stability of the transcripts by promoting interaction with IGF2BP3. This m6A modification was driven by TEAD4-dependent recruitment of the METTL3 methyltransferase complex, identifying TEAD4 as a spatial regulator of m6A deposition. Functionally, METTL3 knockdown in KRAS-mutant syngeneic tumors suppressed tumor growth and restored antitumor immunity by increasing CD8⁺ T-cell and natural killer (NK)–cell infiltration in a CD73-dependent manner. Moreover, METTL3 inhibition synergized with anti-PD-1 therapy and a CD73 inhibitor to reduce tumor burden. Together, these findings demonstrate that KRAS-driven m6A remodeling is a key mechanism of immune suppression in CRC and highlight METTL3 as a promising therapeutic target.
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3. ⭐ GSE311795 KRAS 突变重编程 RNA m6A 修饰以驱动结直肠癌中 CD73 依赖性免疫逃逸 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、scRNA、KRAS
• 📝 描述：Contributors : Seungjae Shin ; Seung-Pyo Hong ; Jong-Il Kim ; Sung-Yup ChoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusKRAS mutations, present in about 40% of colorectal cancers (CRCs), are strongly associated with an immunosuppressive tumor microenvironment characterized by restricted immune infiltration and poor responses to immunotherapy. Here, we show that KRAS mutations remodel the m6A epitranscriptome to promote immune evasion. Methylated RNA-immunoprecipitation sequencing of isogenic CRC cells revealed that KRAS-mutant cells exhibit increased N6-methyladenosine (m6A) deposition on CD73 mRNAs, enhancing the stability of the transcripts by promoting interaction with IGF2BP3. This m6A modification was driven by TEAD4-dependent recruitment of the METTL3 methyltransferase complex, identifying TEAD4 as a spatial regulator of m6A deposition. Functionally, METTL3 knockdown in KRAS-mutant syngeneic tumors suppressed tumor growth and restored antitumor immunity by increasing CD8⁺ T-cell and natural killer (NK)–cell infiltration in a CD73-dependent manner. Moreover, METTL3 inhibition synergized with anti-PD-1 therapy and a CD73 inhibitor to reduce tumor burden. Together, these findings demonstrate that KRAS-driven m6A remodeling is a key mechanism of immune suppression in CRC and highlight METTL3 as a promising therapeutic target.
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4. ⭐ GSE311796 KRAS 突变重编程 RNA m6A 修饰以驱动结直肠癌中 CD73 依赖性免疫逃逸 [MeRIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、KRAS
• 📝 描述：Contributors : Seungjae Shin ; Seung-Pyo Hong ; Jong-Il Kim ; Sung-Yup ChoSeries Type : OtherOrganism : Homo sapiensKRAS mutations, present in about 40% of colorectal cancers (CRCs), are strongly associated with an immunosuppressive tumor microenvironment characterized by restricted immune infiltration and poor responses to immunotherapy. Here, we show that KRAS mutations remodel the m6A epitranscriptome to promote immune evasion. Methylated RNA-immunoprecipitation sequencing of isogenic CRC cells revealed that KRAS-mutant cells exhibit increased N6-methyladenosine (m6A) deposition on CD73 mRNAs, enhancing the stability of the transcripts by promoting interaction with IGF2BP3. This m6A modification was driven by TEAD4-dependent recruitment of the METTL3 methyltransferase complex, identifying TEAD4 as a spatial regulator of m6A deposition. Functionally, METTL3 knockdown in KRAS-mutant syngeneic tumors suppressed tumor growth and restored antitumor immunity by increasing CD8⁺ T-cell and natural killer (NK)–cell infiltration in a CD73-dependent manner. Moreover, METTL3 inhibition synergized with anti-PD-1 therapy and a CD73 inhibitor to reduce tumor burden. Together, these findings demonstrate that KRAS-driven m6A remodeling is a key mechanism of immune suppression in CRC and highlight METTL3 as a promising therapeutic target.
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5. GSE339333 CHI3L1 调控卵巢癌细胞中的基因甲基化修饰

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、methylation
• 📝 描述：Contributor : Yaodi ShaoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensAdipocyte-tumor interaction plays a critical role in tumor microenvironment. Typically, high-grade serous ovarian carcinoma (HGSOC) preferentially metastasizes to the omentum, an adipocyte-rich tissue, and obesity correlates with worse patient prognosis. However, the underlying mechanisms remain poorly understood. Here, we identify a bidirectional adipocyte–cancer cell axis in which HGSOC cells stimulate lactate metabolism in adjacent adipocytes, leading to hypoxia-inducible factor 1α (HIF-1α) activation and subsequent secretion of chitinase 3-like 1 (CHI3L1). On the one hand, CHI3L1 acts as an inflammatory factor that promotes the secretion of additional cytokines, perpetuating omental inflammation, driving CD8⁺ T cell exhaustion, and shaping an immunosuppressive microenvironment that favors tumor metastasis. On the other hand, CHI3L1 binds to and stabilizes protein arginine methyltransferase 5 (PRMT5) in tumor cells, thereby enhancing its methyltransferase activity. This upregulation suppresses dual-specificity phosphatase 1 (DUSP1), a phosphatase of mitogen-activated protein kinase (MAPK), and sustains oncogenic MAPK signaling across multiple tumor models. Obesity amplifies this pathway by heightening HIF-1α activity and elevating CHI3L1 levels in adipose tissue, which drives both tumor progression and resistance to anti-angiogenic therapy. Pharmacological inhibition of CHI3L1 disrupts this signaling loop and restores therapeutic sensitivity, while also alleviating immune exhaustion in the tumor microenvironment. Collectively, our findings establish CHI3L1 as a key mediator of a unified mechanism that drives omental tropism and obesity-associated aggressive phenotypes, highlighting its potential as a prognostic biomarker and therapeutic target to improve anti-angiogenic therapy.
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6. GSE283112 可卡因奖赏相关海马学习中DNA甲基化的大规模重组和细胞外基质基因的上调[RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、methylation
• 📝 描述：Contributors : Madelyn Baker ; Elizabeth Brindley ; Kyle Windisch ; Anjali Rajadhyaksha ; Miklos TothSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCocaine addiction is characterized by compulsive drug use and relapse triggered by drug-related cues and contexts. Though previous research on substance use disorders has primarily focused on the mesolimbic reward pathway, the hippocampus plays an important role in encoding the spatial and contextual features of reward-associated learning. The dorsal dentate gyrus of the hippocampus receives contextual information from the entorhinal cortex and forms the memories of drug-associated contexts in sparse ensembles of dentate granule cells. Since dentate granule cells, unlike other principal hippocampal neurons, express dopamine D1 receptors; they uniquely respond to the extracellular increase of dopamine during cocaine use. Given these inputs, we hypothesized that repeated experience with cocaine during self-administration would produce substantial epigenetic and transcriptional changes in dentate granule cells that, via circuit maladaptation, contributes to the strong and lasting memories of drug experience and to the high incidence of relapse. Here we report DNA methylation changes, biased toward hypomethylation, in dentate granule cells at the unusually high number of ~30,000 small, 100-200 bp genomic regions, while the purely environmental challenge of chronic unpredictable stress produced 10 times fewer differentially methylated regions. Cocaine-sensitive epigenomic regions, in contrast to the rest of the genome, had heterogenous methylation in the otherwise largely homogenous population of mature dentate granule cells, suggesting that their cocaine-induced epigenetic malleability is due to relatively unhindered switching between the methylated and unmethylated states. Further, these regions were overrepresented in enhancers and associated with about half of the expressed genes (~8,000) of diverse gene ontology functions that, however, were not random and had relevance to neuronal plasticity. In contrast, only ~400 genes were upregulated in cocaine self-administration that included a significant number of differentially methylated genes. These genes included many collage genes and were enriched in the functional category of Organization of extracellular matrix (ECM), an extra-neuronal structure involved in neuronal connectivity and plasticity. The DNA methylation and gen…
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7. GSE299520 Ankrd11 缺陷逆转慢性 HBV 特异性 T 细胞功能障碍 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Contributors : Wei Xu ; Xuyu ZhouSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo investigate the transcriptomic changes in CD8 T cells upon Ankrd11 deficiency, we performed RNA-seq to analyze alterations in the transcriptome between Ankrd11-knockout and wild-type CD8 T cells.
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8. GSE299519 Ankrd11 缺陷逆转慢性 HBV 特异性 T 细胞功能障碍 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ATAC-seq
• 📝 描述：Contributors : Wei Xu ; Xuyu ZhouSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTo investigate the impact of Ankrd11 deficiency on chromatin accessibility in CD8 T cells, we performed ATAC-seq to analyze differences in chromatin openness between Ankrd11-knockout CD8 T cells and wild-type CD8 T cells.​​
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9. GSE339419 多组学分析揭示表观遗传和lncRNA变化与早期人类软骨内成骨启动之间的联系

• ✍️ 作者：未知作者
• 🏷️ 关键词：epigenetic
• 📝 描述：Contributors : David Hidalgo Gil ; Paul BourgineSeries Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencingOrganism : Homo sapiensDifferentiation programs remain incompletely understood across stem cell types, including for human bone marrow mesenchymal stromal/stem (BM-MSCs) cells, a heterogenous population orchestrating bone formation and establishing a functional hematopoietic niche in the bone marrow. BM-MSCs form and repair bone through the evolutionarily conserved process of endochondral ossification (EO), initiated by deposition of a transient cartilage template subsequently remodeled into bone and bone marrow tissues. Despite their considerable potential for skeletal regeneration, the early molecular and cellular events underlying BM-MSCs commitment to EO remain elusive. To overcome donor dependent variability in chondrogenic potential that limits mechanistic studies, we here exploit OssiGel as a potent chondro-inductive extracellular matrix offering robust recapitulation of EO by BM-MSCs. Through multi-omics profiling of OssiGel-primed BM-MSCs, we identify rapid chromatin remodeling at chondrogenic loci as concomitant for lineage commitment. The emergence of a chondro-progenitor population is detected as early as 3 days in vivo and correlates with successful EO recapitulation. Mechanistically, we identify LINC02511 as novel enhancer-associated element involved in the onset of EO. We confirm presence of LINC02511 in human skeletal atlases, and its CRISPR-mediated silencing significantly impaired EO. By integrating human tissue engineering strategies with single cell multi-omics profiling, our study provides a framework for deciphering BM-MSCs fate decisions, highlighting the role of enhancer and non-coding elements as key determinants of early lineage specification. These findings advance our understanding of BM-MSCs biology and will prompt their translational exploitation in regenerative medicine.
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10. GSE339404 Aβ42 处理后人类前脑类器官的批量 RNA 测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：Contributor : Yilin FengSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHuman iPSC-derived forebrain organoids were exposed to amyloid-β42 (Aβ42) at day90 to model Alzheimer’s disease-associated pathology. Bulk RNA sequencing was performed to characterize transcriptional changes induced by Aβ42 treatment. The resulting dataset provides genome-wide expression profiles of treated and untreated organoids.
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1. 咖啡或许有助于保护肝脏免受脂肪堆积、瘢痕形成和癌症的侵害。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A major long-term study linked coffee consumption with lower risks of cirrhosis, liver cancer, and death from liver disease. Coffee drinkers also showed healthier liver scans and blood protein patterns, with less fat, inflammation, and scarring. Benefits appeared even at one or two cups daily and were strongest around three to four cups.
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• GSE317736 RNA-seq 分析药物治疗下的大鼠肝脏
• GSE301655 调控变异的单等位基因纳米级定位[RNA-Seq]
• GSE283146 可卡因奖赏相关海马学习中 DNA 甲基化的大规模重组和细胞外基质基因的上调 [RRBS]
• GSE273283 协同超声激活人工酶与精准基因疗法抑制氧化还原稳态和恶性表型以可控对抗肝细胞癌
• GSE307355 人类视网膜色素上皮的三维表观基因组图谱[RNA-seq]
• GSE307354 人类视网膜色素上皮的 3D 表观基因组图谱 [ATAC-seq]
• GSE262645 mregDCs诱导子宫内膜异位症中T细胞功能异常