ONCOGENE癌基因
ONCOGENE(英文缩写 ONCOGENE),ISSN 0950-9232,eISSN 1476-5594,中文译名:癌基因 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 8.756 | Q1 |
| 2022 | 8.000 | Q1 |
| 2023 | 6.900 | Q1 |
| 2024 | 7.300 | Q1 |
| 2025 | 9.100 | Q1 |
ONCOGENE 最新收录文献
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1. KDM4A drives TGCT metastasis by inducing focal adhesion disassembly via STAT1-mediated CCL3 transcriptional activation.
1. KDM4A通过STAT1介导的CCL3转录激活诱导黏着斑分解，从而驱动TGCT转移PMID:日期:2026-10-04Dysregulation of histone demethylation is a pivotal epigenetic event driving malignant tumor progression. Thus, it is critical to understand the downstream signaling pathways that govern dysregulation of histone demethylation. Here, we identified KDM4A as the exclusively and significantly up-regulated member in testicular germ cell tumors (TGCTs) through a pan-family expression screen of histone demethylases (KDM1-8 and JMJD6) using the GEPIA database. KDM4A knockdown markedly inhibits TGCT cell migration and invasion in vitro, and metastatic potential in vivo. Mechanistically, KDM4A induces H3K9me3 demethylation at the CCL3 promoter, thereby restoring chromatin accessibility to facilitate STAT1-dependent CCL3 transcriptional activation, which activates the PI3K/AKT pathway, ultimately promoting focal adhesion turnover and enhancing cellular invasiveness. Furthermore, in a lung metastasis model, KDM4A significantly promoted distal colonization of TGCT in a CCL3-dependent manner. Summary, our findings reveal that KDM4A is a critical epigenetic regulator of TGCT metastasis, driving tumor progression via the STAT1-dependent CCL3 transcriptional activation, which promotes focal adhesion turnover by PI3K/AKT axis. Hence, targeting KDM4A may be a promising therapeutic strategy for improving the clinical prognosis of patients with metastatic TGCT.
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2. Nuclear cathepsin L induces DNA damage by regulating DNA repair factors in ovarian cancer.
2. 核组织蛋白酶L通过调控卵巢癌中的DNA修复因子诱导DNA损伤PMID:日期:2026-10-01Resistance to PARP inhibitors (PARPi) remains a major clinical challenge in ovarian cancer (OC), emphasizing the need for novel strategies to enhance therapeutic efficiency. Our previous work revealed that the antimalarial drug quinacrine (QC) can be repurposed to induce cell death in OC by promoting lysosomal release of active cathepsin L (CTSL). Building on these outcomes, we investigated whether QC-activated CTSL influences DNA damage and homologous recombination (HR) repair in OC cells. Our experimental evidence shows that QC-activated CTSL downregulates key DNA repair proteins RAD51 and 53BP1, leading to impaired HR repair and increased DNA damage. Importantly, genetic knockdown of CTSL significantly reduced QC-induced DNA damage, confirming the CTSL plays a direct functional role in this process. We also found out that the response of combined QC and PARPi differs in models. CTSL was translocated to the nucleus (nCTSL) in responsive patient-derived ascitic (PDA) and patient-derived xenograft (PDX) spheroids. Contrarily, non-responsive models did not have nuclear CTSL. Mechanically, QC could not suppress CRM1/XPO1 nuclear export receptor in non-responsive cells, leading to continued export of CTSL from the nucleus. To address this, we have used the CRM1 inhibitor KPT-8602, which restored nuclear retention of CTSL. This led to enhanced therapeutic synergy with PARPi and overcame resistance in QC-treated PDA 3D-spheroids. Consistent with these findings, QC reduced tumor burden in both the cell-derived OVCAR-5 xenograft and PDX-PH070 models that showed QC-induced nCTSL, but not in the non-responsive PDX-PH095 model. However, in additional non-responsive PDX models (PH747 and PH081), treatment with QC and KPT-8602 substantially reduced tumor burden. Collectively, our results confirm a critical role for nuclear CTSL in QC-induced DNA damage and identify nCTSL as a possible predictive biomarker of therapeutic response. These results suggest that combining QC with PARPi or CRM1 inhibitors represents a promising strategy to overcome PARPi resistance in OC.
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3. KAT5-mediated HSPA1A lactylation drives immunotherapy resistance by inhibiting STAT1 degradation in esophageal squamous cell carcinoma.
3. KAT5介导的HSPA1A乳酸化通过抑制STAT1降解驱动食管鳞状细胞癌的免疫治疗耐药PMID:日期:2026-09-24Immunotherapy has shown promising efficacy in esophageal squamous cell carcinoma (ESCC), yet its clinical benefits remain limited due to immune evasion. Lactate accumulation in the tumor microenvironment has been found to facilitate immune evasion through protein lactylation. However, the key lactylated substrates and mechanisms driving immune evasion remain undefined. Here, we show that HSPA1A lactylation at lysine 108 (K108) by KAT5 drives CD8⁺ T cell dysfunction and immunotherapy resistance via the STAT1/PD-L1 axis in ESCC. Mechanistically, K108 lactylation enhances HSPA1A binding to STAT1, protecting STAT1 from TRIM25-mediated ubiquitination and proteasomal degradation. This stabilization promotes STAT1 phosphorylation and nuclear translocation, leading to transcriptional upregulation of PD-L1 and subsequent immune evasion. Collectively, these findings highlight the pivotal role of HSPA1A lactylation in facilitating immune evasion via the STAT1/PD-L1 axis, suggesting a potential target for improving immunotherapy efficacy in ESCC.
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4. Phylogenetic and phylodynamic approaches to understanding the evolution of non-small cell lung cancer using single-cell sequencing.
PMID:日期:2026-09-24Characterizing the genealogy of tumor cells and their population dynamics is central to our understanding of the evolution of cancer. While direct monitoring of the tumor evolutionary process is impractical, we leverage advances in phylogenetics and phylodynamics to explore the evolutionary dynamics of non-small cell lung cancer (NSCLC) using single-cell whole exome sequencing data from 351 tumor cells across 11 NSCLC patients, predominantly focusing on the primary tumors and early stages of NSCLC. Our results reveal distinct phylogenetic tree shapes and evolutionary trajectories across different stages of NSCLC evolution. However, this intricate and multi-phase evolutionary process cannot be fully elucidated by current tumor models. Herein, we hypothesize that tumors progress through the following phases: (1) an initial rapid expansion through Big Bang-like growth, (2) a prolonged plateau period of non-progression with possible accumulation of neutral substitutions, (3) a subsequent phase where adaptive substitutions accumulate gradually, (4) a bottleneck event where selectively advantageous subclones acquire invasive capabilities (characterized by a pattern of punctuated evolution), and, potentially, a rapid expansion leading to metastasis. This work highlights the use of single-cell phylogenetics and phylodynamics for interpreting the evolution of NSCLC, with potential in predicting cancer progression, resistance mechanisms, and treatment response.
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5. Synonymous codon usage shapes ERα function through specialized translational programs during breast cancer progression.
5. 同义密码子使用通过乳腺癌进展过程中的专门翻译程序塑造ERα功能PMID:日期:2026-09-24Long considered neutral, synonymous codon usage is increasingly recognized as a regulatory layer of mRNA translation. Proteins expressed during proliferation are translated from mRNAs with codon compositions distinct from those encoding proteins in differentiated states, suggesting the existence of specialized translational programs. In hormone-receptor-positive breast cancer, estrogen receptor-alpha (ERα/ESR1) acts both as a driver of proliferation and as a maintainer of luminal identity, making its translational regulation particularly relevant. Here, we show that the transition of breast cancer cells from quiescent, differentiated states towards proliferative, less differentiated phenotypes, is accompanied by a systematic shift from G/C3- to A/U3-biased codon usage. ERα coding sequence architecture mirrors these translational programs through both global codon composition and position-dependent codon patterns. These features influence translational efficiency and likely modulate co-translational folding dynamics, thereby adjusting receptor abundance and functional outputs according to the prevailing translational program. Consistent with their functional importance, synonymous codon choices are subject to increased selective constraints within regions encoding structural and functional domains. Using engineer synonymous ERα variants, we demonstrate that codon usage fine-tunes receptor function across distinct cellular states. Together, our findings identify synonymous codon usage as a previously unrecognized mechanism linking translational programs to ERα expression and function.
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6. SETDB1 cooperates with the CRL4B complex to promote colorectal cancer tumorigenesis by disrupting circadian rhythm.
6. SETDB1与CRL4B复合物协作，通过破坏昼夜节律促进结直肠癌肿瘤发生PMID:日期:2026-09-23The circadian rhythm is an intrinsic, self-regulatory physiological system in organisms that is hierarchically governed by core clock genes. Dysregulation of this rhythm is closely associated with tumor progression. However, the specific molecular mechanisms underlying circadian rhythm disruption-mediated colorectal cancer (CRC) remain largely elusive. The histone methyltransferase SET domain bifurcated 1 (SETDB1) exerts oncogenic functions in multiple solid tumors, prompting this study to investigate the molecular mechanisms through which SETDB1 regulates CRC progression. Our results demonstrate that SETDB1 acts as an oncogene in CRC by interacting with the Cullin 4B-RING E3 ligase (CRL4B) complex to enhance cancer cell proliferation, invasion, and stemness maintenance. Specifically, SETDB1 and the CRL4B complex assemble into a transcriptional repressor complex that binds to the promoters of core clock genes, such as PER3 and CRY1, to repress their transcription, thereby disrupting cellular circadian rhythms and ultimately accelerating CRC cell proliferation and metastasis. Collectively, our findings elucidate the pivotal role of the SETDB1/CRL4B complex in CRC pathogenesis and provide a potential therapeutic strategy targeting SETDB1 for patients with CRC with high CUL4B expression.
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7. DDR1 sustains ferroptosis resistance in pancreatic ductal adenocarcinoma via SLC40A1-mediated iron homeostasis.
7. DDR1通过SLC40A1介导的铁稳态维持胰腺导管腺癌的铁死亡抵抗PMID:日期:2026-09-23Integrated single-cell transcriptomics and clinical analyses reveal elevated DDR1 expression in pancreatic ductal adenocarcinoma (PDAC) tissues, which correlates with poor prognosis. Mechanistically, collagen-activated Discoidin Domain Receptor 1 (DDR1) recruits SHC1 to activate the MAPK/ERK pathway, thereby driving transcriptional upregulation of SLC40A1 via the ERK-MYC axis. SLC40A1, encoding an iron exporter, reduces intracellular labile iron pools, thereby suppressing lipid peroxidation and ferroptosis. Consequently, DDR1 overexpression confers resistance to dihydroartemisinin (DHA)-induced ferroptosis in PDAC cells, characterized by diminished ROS accumulation, mitochondrial shrinkage, and cristae loss. Conversely, DDR1 knockdown or pharmacological inhibition (Dasatinib) sensitizes PDAC cells to DHA. Crucially, combining Dasatinib and DHA treatment synergistically inhibits tumor growth in vivo by reactivating ferroptosis, as evidenced by increased 4-HNE accumulation and decreased Ki67 expression. These findings identify DDR1 as a key regulator of iron metabolism and ferroptosis in PDAC, suggesting that dual targeting of DDR1 and ferroptosis represents a promising therapeutic strategy.
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8. Correction: Splicing-mediated control of hnRNPD isoform switching by SRSF2 drives PD-L1-dependent immune evasion in gallbladder cancer.
8. 更正：SRSF2通过剪接介导的hnRNPD异构体转换调控驱动胆囊癌中PD-L1依赖的免疫逃逸PMID:日期:2026-09-22该文献暂无摘要。
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9. Beyond the blood-brain barrier: humanised mice, the missing link in glioblastoma research.
9. 跨越血脑屏障：人源化小鼠——胶质母细胞瘤研究中缺失的一环PMID:日期:2026-09-20Glioblastoma (GBM) remains a major challenge in neuro-oncology, associated with a high rate of mortality despite decades of intensive research and therapeutic advancements, underscoring the urgent need for innovative preclinical platforms that can more accurately recapitulate the biological and pathological features of human disease. While conventional animal models have contributed to our understanding of GBM biology and the evaluation of treatment efficacy, they fail to capture the full complexity and heterogeneity of the tumour microenvironment (TME). Ex vivo models are associated with certain advantages in this context; however, they can not mirror the complex dynamic and multicellular interactions present in living organisms, particularly the critical treatment barriers unique to the central nervous system: the blood-brain barrier (BBB), blood-cerebrospinal fluid barrier (BCSFB) and blood-meningeal barrier (BMB). In response to these limitations, humanised mouse models have emerged as an advanced platform capable of faithfully mimicking the molecular, pathological and immunological features of human GBM. These models enable the replication of complex in vivo crosstalk between the immune system and the TME, while preserving the relevant treatment barriers that govern drug delivery to the brain. Accumulating evidence indicates that humanised mouse models closely reproduce the infiltration of human immune components into the TME, enabling the study of clinically relevant interactions that contribute to therapeutic resistance and treatment failure in GBM. This review aims to provide a comprehensive and systematic overview of the currently employed humanised mouse models in GBM research, highlighting their applications and comparative advantages. Finally, we evaluate the opportunities and challenges associated with each model and discuss future directions to increase the translational relevance and predictive power of preclinical GBM research. Humanised mouse models provide a valuable translational platform combining the human immune system and PDX orthotopic engraftment. Compared to conventional models and ex vivo models, these models can reproduce the complex cross-talk between tumour cells and the immune system, tumour heterogeneity, immunosuppressive TME, as well as complex in vivo interactions such as brain-specific barriers, including BBB, BCSFB and BMB. Future implementation of the human gut microbiome in these models has the potential to further increase translational relevance and precision in GBM research. Created in BioRender.com.
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10. A canonical role of SMAD4 in safeguarding 3D genome architecture to suppress lung tumorigenesis.
PMID:日期:2026-09-18Dysregulation of three-dimensional (3D) genome architecture is a hallmark of cancer, yet the mechanisms by which its disruption drives tumorigenesis remain incompletely understood. Here, we demonstrated that SMAD4 regulated 3D genome organization through its canonical transcription factor activity by directly binding chromatin, thereby suppressing lung tumorigenesis. Hi-C analyses of human lung tumors identify SMAD4 as a potential regulator of 3D genome integrity. Using PTEN-deficient human bronchial epithelial cells and genetically engineered mouse models, we showed that SMAD4 loss induced widespread reorganization of chromatin compartments, topologically associating domain (TAD) boundaries, and chromatin loops, leading to oncogenic transcriptional rewiring during early tumorigenesis. Mechanistically, SMAD4 directly bound chromatin loops and spatially connected gene promoters with active or repressive regulatory elements to control transcription. Upon SMAD4 ablation, enhancer-promoter rewiring dysregulated critical oncogenic drivers, including ELF3. Functional manipulation of an SMAD4-regulated ELF3-associated chromatin loop altered ELF3 expression and cell survival both in vitro and in vivo. Collectively, our findings establish SMAD4 as a direct regulator of 3D genome architecture through classical transcription factor binding to chromatin loops and reveal enhancer-promoter rewiring as a key mechanism driving lung tumorigenesis and a potential therapeutic vulnerability in SMAD4-deficient lung cancer.