Cancer letters最新文献

{"title":"HNF4A functions as a hepatocellular carcinoma oncogene or tumor suppressor depending upon the AMPK pathway activity status","authors":"Zhaoyu Qin ,&nbsp;Yan Li ,&nbsp;Xiexiang Shao ,&nbsp;Kai Li ,&nbsp;Yihe Bai ,&nbsp;Bing Wang ,&nbsp;Fahan Ma ,&nbsp;Wenhao Shi ,&nbsp;Lei Song ,&nbsp;Aojia Zhuang ,&nbsp;Fuchu He ,&nbsp;Chen Ding ,&nbsp;Wenjun Yang","doi":"10.1016/j.canlet.2025.217732","DOIUrl":"10.1016/j.canlet.2025.217732","url":null,"abstract":"<div><div>Cancer cells frequently undergo energy metabolic stress induced by the increased dynamics of nutrient supply. Hepatocyte nuclear factor 4A (HNF4A) is a master transcription factor (TF) in hepatocytes that regulates metabolism and differentiation. However, the mechanism underlying how HNF4A functions in cancer progression remains unclear due to conflicting results observed in numerous studies. To address the roles of HNF4A in hepatocellular carcinoma (HCC), we investigated the regulatory functions of HNF4A in HCC cells under different glucose supply conditions. We found that HNF4A exhibited tumor-suppressive effects on the proliferation and migration of HCC cells in glucose-sufficient conditions and tumor-promotive effects on HCC cells in glucose-insufficient conditions. Further investigation revealed that this diverse function of HNF4A was dependent upon the AMPK pathway activity. Similarly, the prognosis predicted by HNF4A was also correlated with whether the AMPKa expression levels were low or high in clinical HCC patients. Multiomics approaches consisting of proteomics and ChIP-seq revealed that key HNF4A target genes, including NEDD4 and RPS6KA2, are involved in the diverse function of HNF4A in HCC in response to the AMPK activity status. Specifically, HNF4A could bind to the promoter region of NEDD4 and RPS6KA2, and upregulating their expression. Our study has demonstrated the relationship between and synergism of AMPK and HNF4A in the progression of HCC under diverse nutrient conditions.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217732"},"PeriodicalIF":9.1,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143858982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The m6A hypermethylation-induced PIR overexpression regulates H3K4me3 and promotes tumorigenesis of uveal melanoma","authors":"Hao Tian ,&nbsp;Ying Chen ,&nbsp;Xiaokang Dong ,&nbsp;Xianqun Fan ,&nbsp;Ruobing Jia","doi":"10.1016/j.canlet.2025.217729","DOIUrl":"10.1016/j.canlet.2025.217729","url":null,"abstract":"<div><div>Uveal melanoma (UM) is the most common primary ocular malignancy in adults, characterized by high mortality, strong metastatic potential, and limited treatment options, necessitating the identification of novel therapeutic targets. Here, we identified Pirin (PIR) as a key oncogenic factor in UM through comprehensive multi-omics analyses, revealing that PIR is significantly upregulated and correlates with poor prognosis. Functional assays indicated that inhibiting PIR markedly suppressed UM progression, highlighting its critical role in tumorigenesis behavior. Mechanistically, PIR expression is driven by aberrant N6-methyladenosine (m⁶A) modifications mediated by METTL3 and IGF2BP3. Meanwhile, the high expressed PIR acts as a transcriptional co-regulator by interacting with WDR5, resulting in the regulation of H3K4me3 modifications at the ANAPC10 promoter region and subsequent promotion of ANAPC10 expression. Overall, our study uncovered the METTL3/IGF2BP3 (m6A)-PIR-WDR5 (H3K4me3)-ANAPC10 axis, bridging RNA methylation and histone methylation in UM pathogenesis. By unmasking these intricate epigenetic interactions, we provided novel insights into <span>UM</span> biology and identified potential therapeutic targets for tumor treatment, offering the theoretical support for future drug development and clinical applications.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217729"},"PeriodicalIF":9.1,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143868222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SENP1-Sirt3 axis promotes cholesterol biosynthesis in tumor-associated macrophages to suppress anti-tumor immunity","authors":"Guoyuan Peng ,&nbsp;Xinyu Yang ,&nbsp;Jianli He ,&nbsp;Mingming Zhang ,&nbsp;Kexin Liu ,&nbsp;Jun Tu ,&nbsp;Hongsheng Tan ,&nbsp;Innocent Agida ,&nbsp;Wei Zhou ,&nbsp;Jinke Cheng ,&nbsp;Tianshi Wang","doi":"10.1016/j.canlet.2025.217728","DOIUrl":"10.1016/j.canlet.2025.217728","url":null,"abstract":"<div><div>Tumor-associated macrophages (TAMs) play a multifaceted role in the tumor microenvironment, notably by suppressing antitumor immune responses through immunosuppressive mechanisms. TAMs secrete a range of cytokines that simultaneously inhibit T cell function and foster a microenvironment that supports tumor progression and dissemination. Our study has delved into the intricate relationship between the metabolic reprogramming of TAMs and their impact on tumor progression. Mitochondrial metabolic reprogramming mediated by the SENP1-Sirt3 axis altered the dynamics and activity of tumor-infiltrating immune cells, including macrophages and CD8⁺ T lymphocytes. SENP1-Sirt3 axis increases the level of acetyl-CoA in macrophage mitochondria, which in turn promotes cholesterol biosynthesis in macrophages. The upregulation of cholesterol synthesis is a key factor in driving macrophage polarization towards the immunosuppressive M2 phenotype, which in turn supports tumor development. Notably, increased cholesterol levels contributed to a reduction in the number and activity of CD8⁺ T cells, which are essential for mounting an effective immune response against cancer cells. These findings suggest that targeting cholesterol biosynthesis in TAMs may be a promising strategy for cancer immunotherapy.</div></div><div><h3>Significance</h3><div>Activation of the SENP1-Sirt3 axis initiates mitochondrial metabolic reprogramming in tumor-associated macrophages (TAMs), leading to enhanced cholesterol and acetyl-CoA production, M2 macrophage polarization, and impaired CD8⁺ T cell anti-tumor responses.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217728"},"PeriodicalIF":9.1,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143878787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiplex characterization of circulating tumor cells from ductal carcinoma in situ patients suggests early tumor dissemination","authors":"Brittany Rupp ,&nbsp;Neha Nagpal ,&nbsp;Brooke Thanasiu ,&nbsp;Kristen Tuck ,&nbsp;Kirk Herman ,&nbsp;Dean E. Brenner ,&nbsp;Justin Colacino ,&nbsp;Max Wicha ,&nbsp;Sunitha Nagrath","doi":"10.1016/j.canlet.2025.217703","DOIUrl":"10.1016/j.canlet.2025.217703","url":null,"abstract":"<div><div>While ducal carcinoma in situ (DCIS) is considered to be pre-invasive, some patients will develop metastatic disease after a long disease-free interval. The prevailing dogma posits that invasive local recurrence is the source of subsequent metastasis, and thus the goal of DCIS therapy is the prevention of local recurrence. Recently, this paradigm has been called into question by the observation that some women develop metastatic disease in the absence of local recurrence or even following bilateral mastectomies, suggesting early cancer dissemination in some patients. If the presence of circulating tumor cells (CTCs) can be verified on some patients with pure DCIS, then dissemination may be occurring earlier than previously thought, suggesting that these patients might require additional monitoring or treatment. Here, we present a workflow to isolate and characterize CTCs from DCIS patients. Using a high throughput size based inertial focusing microfluidic device, the Labyrinth, we isolated and identified CTCs in 66.6 % (12/18) of DCIS patients with an average of 1.337 CTCs per five mL. Immunofluorescence staining and single cell qPCR of CTCs reveal mesenchymal characteristics of the cells that may contribute to their ability to migrate and metastasize. Preliminary targeted DNA sequencing revealed single nucleotide variations previously found in DCIS samples. Overall, this data supports the hypothesis that cancer dissemination is occurring in a subset of DCIS patients earlier than previously thought. Additionally, the molecular characterization of CTC in DCIS patients may provide important information on their biological characteristics and associated clinical behavior.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217703"},"PeriodicalIF":9.1,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATF4:p52 complex activates oncogenic enhancers in multiple myeloma via p300/CBP recruitment to regulate BACH1","authors":"Daniel Aron Ang ,&nbsp;Nathan Harmston ,&nbsp;Yinghui Li","doi":"10.1016/j.canlet.2025.217727","DOIUrl":"10.1016/j.canlet.2025.217727","url":null,"abstract":"<div><div>Multiple myeloma (MM) is a B-cell malignancy accounting for 20 % of all blood-associated cancers. MM patients with a poorer prognosis and high-risk stratification were previously observed to be causally linked to the constitutive activation of non-canonical NF-κB (ncNF-κB) pathway. Consistent with this, the ncNF-κB p52 transcription factor was earlier found to regulate the enhancer landscape of MM to potentiate oncogenic transcription. However, the mechanism by which aberrant p52 expression is involved in coordinating enhancer activity has not been well explored. In this study, we analysed H3K27ac ChIP-seq and ATAC-seq data from MM cell lines and patient samples to screen for putative transcription factors that cooperate with p52 to regulate enhancers activated in MM. We report that ATF4 interacts with p52 and together, this complex mediates the activity of a subset of MM-associated enhancers through the recruitment of histone acetyltransferases (HATs), p300 and CBP (CREB-binding protein). We also identified a ATF4:p52 regulated target gene <em>BACH1</em> under the regulation of a proximal super-enhancer, which was found to drive oncogenesis in MM by promoting cell cycle progression and proliferation. Together, our findings provide further mechanistic insights into how aberrant enhancer activation observed in MM tumours could lead to disease progression.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217727"},"PeriodicalIF":9.1,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143895635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIK1 promotes ferroptosis resistance in pancreatic cancer via HDAC5-STAT6-SLC7A11 axis","authors":"Hao Zhang ,&nbsp;Tao Ma ,&nbsp;Xiaofeng Wen ,&nbsp;Jianlong Jiang ,&nbsp;Jing Chen ,&nbsp;Junfeng Jiang ,&nbsp;Jiancong Xie ,&nbsp;Taiwei Mo ,&nbsp;Ruibing Li ,&nbsp;Hanlin Xie ,&nbsp;Guanzhan Liang ,&nbsp;Lin Wang ,&nbsp;Zheyu Zheng ,&nbsp;Xiaoming Huang ,&nbsp;Chuanyuan Liu ,&nbsp;Yimamu Baihetiyaer ,&nbsp;Abuduhalike Abulimiti ,&nbsp;Xiaosheng He ,&nbsp;Zexian Chen ,&nbsp;Tuo Hu ,&nbsp;Weidong Pan","doi":"10.1016/j.canlet.2025.217726","DOIUrl":"10.1016/j.canlet.2025.217726","url":null,"abstract":"<div><div>The activation of protein kinases is ubiquitous in pancreatic ductal adenocarcinoma (PDAC), yet its impact on ferroptosis remains unclear. SIK1 was identified as a key regulator of ferroptosis resistance in PDAC by kinase database screening. Targeting SIK1 could significantly reverse ferroptosis resistance and enhance cytotoxic effects of gemcitabine via increasing ferroptosis sensitivity in PDAC cells. Mechanistically, SIK1 phosphorylated HDAC5 at Ser498 residue and promoted its interaction with 14-3-3 protein, which further protected HDAC5 from TRIM28-mediated ubiquitylation and degradation. SIK1-stabilized HDAC5 deacetylated STAT6 and enhanced its transcriptional activity to upregulate SLC7A11 expression, ultimately rendering PDAC cells resistance to ferroptosis. SIK1 inhibitor (YKL-05-099) could synergistically enhance the antitumor effects of gemcitabine in organoid and patient-derived xenograft (PDX) models by inducing ferroptosis, suggesting a novel therapeutic target for PDAC. Clinically, SIK1 was positively correlated with SLC7A11 expression in PDAC specimens, which was associated with poor prognosis. These findings unveil a crucial mechanism through which PDAC counters ferroptosis via SIK1-mediated HDAC5 stabilization and subsequent SLC7A11 upregulation. This study underscores the promising potential of targeting SIK1-HDAC5 axis as a therapeutic strategy to overcome drug resistance in PDAC.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217726"},"PeriodicalIF":9.1,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143878788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of the first-line immune checkpoint inhibitor plus chemotherapy for gastroesophageal cancer: A meta-analysis of phase III trials including unreported PD-L1 subgroups","authors":"Choong-kun Lee ,&nbsp;Sejung Park ,&nbsp;Yaeji Lee ,&nbsp;Choa Yun ,&nbsp;Moonki Hong ,&nbsp;Chung Mo Nam ,&nbsp;Hyun Cheol Chung ,&nbsp;Sun Young Rha","doi":"10.1016/j.canlet.2025.217718","DOIUrl":"10.1016/j.canlet.2025.217718","url":null,"abstract":"<div><div>The treatment paradigm for gastroesophageal cancers is evolving with immune checkpoint inhibitors (ICIs) as first-line therapy, making it crucial to understand their efficacy across patient subgroups, especially concerning PD-L1 expression. We performed a meta-analysis of Phase III randomized controlled trials targeting the effectiveness of ICIs with or without chemotherapy for advanced/metastatic HER2-negative gastroesophageal adenocarcinoma (GEA) or esophageal squamous cell carcinoma (ESCC). Kaplan-Meier (KM) curves of all-comer populations and subgroups according to reported PD-L1 cut-offs were extracted from published reports. Using KMSubtraction algorithm, unreported PD-L1 subgroup survival data were reconstructed by utilizing published KM survival curves. Thirteen first-line phase III RCTs involving 11,795 patients with GEA or ESCC were included. For GEA, ICI with or without chemotherapy showed longer OS in patients with PD-L1 combined positive score ≥1 (HR 0.77, 95 % confidence intervals [CI] 0.71–0.83 for ICI plus chemotherapy; HR 0.86, 95 %CI 0.75–1.01 for ICI alone) compared to chemotherapy alone, showing less benefits in low PD-L1 subgroups. ICI, with or without chemotherapy displayed survival benefits among PD-L1 tumor proportion score ≥1 % for ESCC (HR 0.62, 95 %CI 0.52–0.74 for ICI plus chemotherapy; HR 0.67, 95 %CI 0.54–0.84 for ICI alone) compared to chemotherapy alone. ICI combinations were similarly beneficial for Asian and global patients with GEA or ESCC. In conclusion, this meta-analysis, which includes unreported PD-L1 subgroups show benefit of ICIs with or without chemotherapy as a first-line treatment for advanced gastroesophageal cancers, particularly among patients with high PD-L1 expression.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217718"},"PeriodicalIF":9.1,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Colorectal cancer peritoneal metastasis is promoted by tissue-specific fibroblasts that can arise in response to various local disorders.","authors":"Cristiano Ramos, Natalie Walterskirchen, Viktoria Knöbl, Chiara Zotter, Catharina Müller, Vasileios Gerakopoulos, Anna Rauch, Lena Falk, Monika Sachet, Edoardo D'Angelo, Marco Agostini, Dietmar Pils, Stefanie Aust, Michael Grusch, Rebecca Herzog, Klaus Kratochwill, Solange Le Blanc, Kristiaan J Lenos, Louis Vermeulen, Stefan Riss, Thomas Bachleitner-Hofmann, Oliver Strobel, Helmut Dolznig, Michael Bergmann, Christine Brostjan, Lukas W Unger, Rudolf Oehler","doi":"10.1016/j.canlet.2025.217686","DOIUrl":"https://doi.org/10.1016/j.canlet.2025.217686","url":null,"abstract":"<p><p>Peritoneal membrane injury induces the activation of local fibroblasts and tissue remodelling, which ultimately can progress to fibrosis. Metastasis of colorectal cancer (CRC) to the abdominal cavity results in such peritoneal damage. Patients with colorectal cancer peritoneal metastasis (CPM) have a particularly poor prognosis, and CPM tumours are characterised by a high infiltration of fibroblasts. Here, we characterised the molecular and functional features of these fibroblasts, and investigated their interaction with other cells in the peritoneal microenvironment. Primary fibroblasts were isolated from 89 patients with different malignant and benign disorders of the peritoneum. We performed comprehensive analyses of single-cell and transcriptome profiling, secretome characterization, and functional enzymatic activity. We were able to identify a peritoneum-specific fibroblast population that increases in response to different types of damage-inducing peritoneal pathologies, including metastasis. These fibroblasts are characterised by the IGFBP2-dependent expression of CD38, which mediates extracellular non-canonical adenosinergic activity and contributes to the suppression of macrophages and T cells. Importantly, peritoneal fibroblasts promoted the growth and invasiveness of tumour cells in a xenograft mouse model of peritoneal metastasis, highlighting their pro-tumorigenic role. Their specific gene signature was associated with poor prognosis in a dataset of 51 patients suffering from colorectal peritoneal metastasis. This study revealed that the CPM is infiltrated by a peritoneal fibroblast subtype, which is absent in healthy tissue, but also observed in benign peritoneal diseases. Given the limited therapeutic options for these patients, these pro-tumorigenic peritoneal fibroblasts could represent an attractive target for inhibiting the peritoneal spread of tumour cells.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"217686"},"PeriodicalIF":9.1,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HDAC4 super-enhancer drives CEBPB-mediated TWIST2 transcription to promote chemoresistance in LUAD","authors":"Min Jiang ,&nbsp;Kai Zhang ,&nbsp;Guohao Wei ,&nbsp;Feng Qi ,&nbsp;Danlei Yu ,&nbsp;Jingjing Ma ,&nbsp;Xiaofei Zhang ,&nbsp;Longbang Chen ,&nbsp;Yuhao Xie ,&nbsp;Zhengyuan Yu ,&nbsp;Jing Chen ,&nbsp;Dongqin Chen","doi":"10.1016/j.canlet.2025.217716","DOIUrl":"10.1016/j.canlet.2025.217716","url":null,"abstract":"<div><div>Lung cancer remains one of the most prevalent malignancies worldwide. This study investigates the role of histone deacetylase 4 (HDAC4) in mediating chemoresistance in lung adenocarcinoma (LUAD). Super-enhancers (SEs), known to regulate aberrant gene expression, are critical drivers of tumor progression. We identified a specific super-enhancer region associated with HDAC4, referred to as HDAC4-SE. Among its nearby genes, TWIST2 emerged as a key player, strongly linked to chemoresistance and the epithelial-to-mesenchymal transition (EMT). We demonstrated that HDAC4-SE regulates TWIST2 expression, thereby contributing to chemoresistance in LUAD.</div><div>Through bioinformatics analysis, we identified transcription factors binding to both the promoter of TWIST2 and the activation region of HDAC4-SE, with CCAAT/enhancer-binding protein beta (CEBPB) identified as a central regulator. Chromatin immunoprecipitation (ChIP) assays confirmed that CEBPB binds to both the HDAC4-SE and the TWIST2 promoter. Additionally, our investigation into the involvement of long non-coding RNAs (lncRNAs) revealed that LINC01940 might mediate the regulatory effects of HDAC4-SE on downstream genes. In conclusion, we uncovered a novel HDAC4-SE/LINC01940/CEBPB/TWIST2 signaling pathway that drives chemoresistance and tumor progression in LUAD. This pathway offers promising insights into potential therapeutic targets to overcome chemoresistance in lung cancer.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"623 ","pages":"Article 217716"},"PeriodicalIF":9.1,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"VGLL4 deficiency in T cells promotes tumor initiation and progression","authors":"Ningxia Zhang ,&nbsp;Xiaochun Fei ,&nbsp;Jing Wen ,&nbsp;Lei Zhang ,&nbsp;Xiaolong Liu ,&nbsp;Bing Sun ,&nbsp;Kai Wang ,&nbsp;Xue Wang ,&nbsp;Hongbin Ji","doi":"10.1016/j.canlet.2025.217682","DOIUrl":"10.1016/j.canlet.2025.217682","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"622 ","pages":"Article 217682"},"PeriodicalIF":9.1,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}