Cancer letters最新文献_第5页

Neurodegeneration of local sympathetic inputs promotes colorectal cancer progression 局部交感神经输入的神经变性促进结直肠癌的进展

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-22 DOI: 10.1016/j.canlet.2025.217817

Xin Chen , Ying Cao , Yifei Zhao , Yao Ma , Xiangchao Shi , Junwei Wang , Zhaoyu Jiang , Renjie Luo , Zhangyuzi Deng , Xin Zhou , Jing Yang , Wei Fu

{"title":"Neurodegeneration of local sympathetic inputs promotes colorectal cancer progression","authors":"Xin Chen , Ying Cao , Yifei Zhao , Yao Ma , Xiangchao Shi , Junwei Wang , Zhaoyu Jiang , Renjie Luo , Zhangyuzi Deng , Xin Zhou , Jing Yang , Wei Fu","doi":"10.1016/j.canlet.2025.217817","DOIUrl":"10.1016/j.canlet.2025.217817","url":null,"abstract":"<div><div>The nervous system can profoundly influence cancer prognosis, and this frontier of cancer neuroscience has increasingly garnered research attention. However, the involvement of neural signals in colorectal cancer remains incompletely understood. In this study, we exploit advanced three-dimensional imaging and conventional immunohistochemistry to observe a transitional loss of local sympathetic inputs from colorectal adenomas to adenocarcinomas in human patients. This negative correlation similarly occurs in the mouse models of colorectal cancer. Of importance, the pharmacologic ablation of sympathetic innervations significantly exaggerates the progression of colorectal tumors in the chemical-induced mouse model. We then demonstrate that the sympathetic neurotransmitter norepinephrine acts via α2-adrenergic receptors to elevate the cancer cell expression of chemokines to recruit CD8<sup>+</sup> T cells, and the destruction of sympathetic signals leads to their reduction within the tumor microenvironment. Together, these results have elucidated a novel aspect of the neurodegeneration of local sympathetic inputs in promoting colorectal cancer progression.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217817"},"PeriodicalIF":9.1,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144123858","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}

引用次数: 0

Paricalcitol plus hydroxychloroquine enhances gemcitabine activity and induces mesenchymal to epithelial transition in pancreatic ductal adenocarcinoma: A single cell RNA-seq analysis Paricalcitol + hydroxychloroquine增强吉西他滨活性，诱导胰腺导管腺癌间充质向上皮转化：单细胞RNA-seq分析。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-21 DOI: 10.1016/j.canlet.2025.217809

Ganji Purnachandra Nagaraju , Madhu Sudhana Saddala , Sujith Sarvesh , Dhana Sekhar Reddy Bandi , Ateeq M. Khaliq , Ashiq Masood , Mehmet Akce , Bassel F. El-Rayes

{"title":"Paricalcitol plus hydroxychloroquine enhances gemcitabine activity and induces mesenchymal to epithelial transition in pancreatic ductal adenocarcinoma: A single cell RNA-seq analysis","authors":"Ganji Purnachandra Nagaraju , Madhu Sudhana Saddala , Sujith Sarvesh , Dhana Sekhar Reddy Bandi , Ateeq M. Khaliq , Ashiq Masood , Mehmet Akce , Bassel F. El-Rayes","doi":"10.1016/j.canlet.2025.217809","DOIUrl":"10.1016/j.canlet.2025.217809","url":null,"abstract":"<div><div>Epithelial-mesenchymal transition (EMT) describes a process by which epithelial cells acquire mesenchymal properties associated with increased migration, invasion, and resistance to therapy. In pancreatic ductal adenocarcinoma (PDAC), targeting the molecular and intercellular communication pathways that drive EMT represents a promising therapeutic strategy. Here, we investigate the effects of combined treatment with gemcitabine (G), paricalcitol (P), and hydroxychloroquine (GPH) in KPC-Luc orthotopic mouse models of PDAC, using single-cell RNA sequencing (scRNA-seq), high-dimensional weighted gene co-expression network analysis (hdWGCNA), and cell-cell communication analysis. GPH treatment reduces EMT, which is associated with the downregulation of the essential gene fibronectin (<em>Fn1)</em>. Collagen and Fn1 pathways co-expression decreases in GPH-treated KPC-Luc tumors. Cancer-associated fibroblasts (CAFs) appear dominant in collagen signaling, whereas macrophages mediate Fn1 signaling. GPH treatment reduces the expression interaction strength between ligands and receptors (collagen-integrin and <em>Fn1-Cd44</em> or <em>Fn1-Sdc4</em>) compared to sham, PH, and G. Altogether, this study presents a comprehensive single-cell resolution map of the molecular and cellular mechanisms by which GPH treatment impairs EMT in PDAC, identifying potential therapeutic targets within the fibronectin and collagen signaling axes.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217809"},"PeriodicalIF":9.1,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132202","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}

引用次数: 0

A previously uncharacterized role of TAp73 in ferroptosis by modulating oxidative homeostasis in cervical cancer TAp73通过调节宫颈癌中的氧化稳态在铁下垂中的先前未被描述的作用。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-21 DOI: 10.1016/j.canlet.2025.217815

Yafan Gong , Wenxin Zhang , Xingwen Wang , Shanliang Zheng , Hao Liu , Qingyu Lin , Meiqi Wang , Jiangwen Ma , Yi Zhang , Tianyu Li , Ying Hu

{"title":"A previously uncharacterized role of TAp73 in ferroptosis by modulating oxidative homeostasis in cervical cancer","authors":"Yafan Gong , Wenxin Zhang , Xingwen Wang , Shanliang Zheng , Hao Liu , Qingyu Lin , Meiqi Wang , Jiangwen Ma , Yi Zhang , Tianyu Li , Ying Hu","doi":"10.1016/j.canlet.2025.217815","DOIUrl":"10.1016/j.canlet.2025.217815","url":null,"abstract":"<div><div>While the tumor-suppressive functions of p53 are well established, the role of its homolog, TAp73, in cancer remains incompletely characterized and is a subject of active investigation. In this study, we observed downregulation of TAp73 protein expression in cervical cancer tissues, which significantly correlated with adverse clinical outcomes. Through co-expression network analysis, we identified functional associations between TAp73 and key pathways involved in lipid metabolism and redox homeostasis-both critical regulators of ferroptosis, an iron-dependent form of programmed cell death mediated by lipid peroxidation. Mechanistically, we demonstrate that TAp73 promotes ferroptosis by directly upregulating the transcription of β-transducin repeat-containing protein (β-TRCP), thereby facilitating the ubiquitin-dependent degradation of nuclear factor erythroid 2-related factor 2 (NRF2), a master regulator of cellular antioxidant defenses. This TAp73-mediated suppression of NRF2 activity renders cells more susceptible to ferroptotic death. Furthermore, TAp73 expression is transcriptionally induced during ferroptosis through the combined inactivation of enhancer of zeste homolog 2 (EZH2), a core component of polycomb repressive complex 2, and activation of E2F transcription factor 1 (E2F1). Notably, pharmacological inhibition of EZH2 synergized with sulfasalazine (SAS) to enhance ferroptosis in vivo, an effect largely dependent on TAp73. Together, these findings delineate a novel ferroptosis regulatory axis-EZH2/TAp73/β-TRCP/NRF2-and highlight its potential as a therapeutic target for cervical cancer intervention.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"627 ","pages":"Article 217815"},"PeriodicalIF":9.1,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132183","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}

引用次数: 0

N-acetyl-L-cysteine promoted hematopoietic recovery in patients with acute myeloid leukemia after complete remission--A pilot study n-乙酰- l-半胱氨酸促进急性髓系白血病患者完全缓解后的造血功能恢复——一项初步研究

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-20 DOI: 10.1016/j.canlet.2025.217812

Li-Juan Hu , Chen-Yuan Li , Tong Xing , Yu Wang , Qian Jiang , Hao Jiang , Jing Wang , Fei-fei Tang , Ying-Jun Chang , Xiao-Hui Zhang , Yuan Kong , Xiao-Jun Huang

{"title":"N-acetyl-L-cysteine promoted hematopoietic recovery in patients with acute myeloid leukemia after complete remission--A pilot study","authors":"Li-Juan Hu , Chen-Yuan Li , Tong Xing , Yu Wang , Qian Jiang , Hao Jiang , Jing Wang , Fei-fei Tang , Ying-Jun Chang , Xiao-Hui Zhang , Yuan Kong , Xiao-Jun Huang","doi":"10.1016/j.canlet.2025.217812","DOIUrl":"10.1016/j.canlet.2025.217812","url":null,"abstract":"<div><div>Chemotherapy is a cornerstone treatment for acute leukemia (AL), but it often results in bone marrow (BM) failure, leading to infections, anemia, and bleeding, which significantly impact patient survival. Endothelial progenitor cells (EPCs) are critical elements of the BM microenvironment and are essential for hematopoiesis. Our previous research using <em>in vitro</em> and AML mouse models indicated that BM EPC dysfunction, characterized by impaired angiogenesis and elevated reactive oxygen species (ROS) levels in AML patients, could be partially reversed after complete remission (CR) and further improved with N-acetyl-L-cysteine (NAC) treatment. This pilot cohort study (NCT06024031, <span><span>www.clinicaltrials.gov</span><svg><path></path></svg></span>) evaluated the effects of NAC on hematopoietic recovery in 30 newly diagnosed AML patients after induction chemotherapy, compared to a propensity-matched control group of 60 patients. Patients received oral NAC (400 mg, three times daily) for 28 days post-chemotherapy alongside standard supportive care. NAC treatment did not affect CR rates (90 % vs. 80 %, <em>P</em> = 0.23), but significantly shortened platelet recovery time (19 vs. 22 days, <em>P</em> = 0.0001) among CR patients. NAC improved EPC percentages, reduced ROS, and enhanced EPC hematopoiesis-supporting functions in patients who achieved CR. NAC was safe and effective in promoting normal hematopoiesis recovery in AML patients in CR following chemotherapy.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217812"},"PeriodicalIF":9.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107464","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}

引用次数: 0

Aberrant PLAC8 expression characterizes glioblastoma with temozolomide resistance and an immunosuppressive microenvironment 具有替莫唑胺耐药和免疫抑制微环境的胶质母细胞瘤的异常PLAC8表达

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-19 DOI: 10.1016/j.canlet.2025.217805

Han She , Tian-Ran Li , Guozhi Zhao , Liang Yi , Qing Liu , Zheng-Chao Liu , Hao-Yu Pei , Xunjia Li , Deyu Zuo , Qingxiang Mao , Yong Li

{"title":"Aberrant PLAC8 expression characterizes glioblastoma with temozolomide resistance and an immunosuppressive microenvironment","authors":"Han She , Tian-Ran Li , Guozhi Zhao , Liang Yi , Qing Liu , Zheng-Chao Liu , Hao-Yu Pei , Xunjia Li , Deyu Zuo , Qingxiang Mao , Yong Li","doi":"10.1016/j.canlet.2025.217805","DOIUrl":"10.1016/j.canlet.2025.217805","url":null,"abstract":"<div><div>Glioblastoma (GBM), Isocitrate Dehydrogenase-wildtype (IDH-WT) represents the most prevalent and clinically aggressive subtype of adult diffuse gliomas, typically associated with poor prognosis. Temozolomide (TMZ) remains the first-line chemotherapeutic agent for GBM; however, the emergence of TMZ resistance represents a major therapeutic obstacle in clinical practice. This study identifies placenta-specific 8 (PLAC8) as a novel mediator of TMZ resistance in IDH-WT GBM. Elevated PLAC8 expression was strongly correlated with poorer survival rates, higher tumor grades in glioma, establishing it as an independent prognostic factor. Notably, consistent upregulation of PLAC8 was observed in both TMZ-resistant GBM cells and TMZ-treated patients, suggesting its potential as a biomarker for TMZ resistance. Mechanistic studies revealed that PLAC8 regulates TMZ sensitivity in GBM cells through the AKT-mTOR signaling pathway. Additionally, integrated bioinformatics and clinical analyses demonstrated that PLAC8 expression positively correlates with immune cell infiltration while promoting an immunosuppressive tumor microenvironment and modulating immunotherapy-related biomarkers, suggesting its potential as a predictive biomarker for immunotherapy response. In conclusion, PLAC8 represents a promising biomarker and therapeutic target for overcoming TMZ resistance and guiding immunotherapy in GBM. This study provides valuable insights for the development of personalized treatment strategies aimed at improving patient outcomes.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217805"},"PeriodicalIF":9.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107463","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}

引用次数: 0

SMARCA4: Promises and challenges in the treatment of cancers SMARCA4：癌症治疗的希望和挑战

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-19 DOI: 10.1016/j.canlet.2025.217811

Wei Ye , Ding An , Wen-Bin Ou

{"title":"SMARCA4: Promises and challenges in the treatment of cancers","authors":"Wei Ye , Ding An , Wen-Bin Ou","doi":"10.1016/j.canlet.2025.217811","DOIUrl":"10.1016/j.canlet.2025.217811","url":null,"abstract":"<div><div>The SWI/SNF (switch/sucrose non-fermentable) related BAF (BRG1/BRM-related factor) chromatin remodeling complex subunit ATPase 4 (<em>SMARCA4</em>) is a gene with a high mutation frequency in the SWI/SNF complex. It plays a role as an ATP-dependent catalytic subunit, participates in remodeling chromatin structure and regulation of gene expression, and is closely related to the poor prognosis of malignant tumors. It is imperative to conduct a comprehensive investigation into the distinctive biological functions and mechanisms by which SMARCA4 contributes to cancer development and to devise targeted therapeutic strategies. Despite numerous studies associating SMARCA4 with the regulation of essential genes, ferroptosis, autophagy, lipid metabolism, and oxidative stress, the precise mechanisms of SMARCA4 in tumors remain unclear. Patients with <em>SMARCA4</em> mutations exhibit a poor prognosis and demonstrate limited responsiveness to surgery, targeted therapies, immunotherapy, and chemotherapies. Thus, SMARCA4 emerges as a promising biomarker and therapeutic target. However, the development of more effective precision therapy tools remains an urgent unmet need. The unique molecular characteristics of SMARCA4 pose significant challenges for targeted drug development. Notably, the discovery of inhibitors targeting SMARCA4 synthetic lethal partners and associated pathways has marked a breakthrough in this field. Monotherapies directed against SMARCA4 face several limitations, including drug resistance, suboptimal objective response rates, and dose-limiting toxicities. Consequently, the exploration of combinatorial therapeutic strategies for SMARCA4 deficiency populations represents a critical direction for future clinical translation.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217811"},"PeriodicalIF":9.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107462","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}

引用次数: 0

Ketogenesis instigates immune suppression in enzalutamide resistant prostate cancer via OTUD7B β-hydroxybutyrylation 生酮通过OTUD7B β-羟基丁基化激活恩杂鲁胺耐药前列腺癌的免疫抑制。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-18 DOI: 10.1016/j.canlet.2025.217808

Haoran Jiang , Yuan Zeng , Weiqiang Ning , Junkai Hong , Moyang Zhu , Ping Li , Fangdie Ye , Zhifa Chen , Haoran Chen , Wei Chen , Gang Li , Hang Huang

{"title":"Ketogenesis instigates immune suppression in enzalutamide resistant prostate cancer via OTUD7B β-hydroxybutyrylation","authors":"Haoran Jiang , Yuan Zeng , Weiqiang Ning , Junkai Hong , Moyang Zhu , Ping Li , Fangdie Ye , Zhifa Chen , Haoran Chen , Wei Chen , Gang Li , Hang Huang","doi":"10.1016/j.canlet.2025.217808","DOIUrl":"10.1016/j.canlet.2025.217808","url":null,"abstract":"<div><div>Next-generation androgen receptor inhibitors are the primary treatment for metastatic prostate cancer. Unfortunately, the majority of patients rapidly develop resistance. Resistance to enzalutamide has been linked to the emergence of an immunosuppressive tumor, although the underlying mechanisms remain poorly understood. In this study, we observed a marked overexpression of enzymes involved in the ketogenic pathway in enzalutamide-induced castration-resistant prostate cancer, which contributed to immune desertification and resistance to immunotherapy. Mechanistically, upregulation of the ketogenic pathway led to the accumulation of β-hydroxybutyrate, which promoted β-hydroxybutyrylation of the cell cycle-regulated deubiquitinase OTUD7B at lysine 511. This modification impaired the degradation of APC/C substrates, resulting in a subsequent reduction in cytoplasmic double-stranded DNA accumulation, thereby attenuating cGAS-STING activation and interferon expression. These findings shed light on the metabolic adaptations and immune escape driven by androgen receptor signaling inhibitors, potentially informing the development of more effective and durable therapeutic approaches in the near future.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217808"},"PeriodicalIF":9.1,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109736","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}

引用次数: 0

Preferential release of microRNAs via extracellular vesicles is associated with ductal carcinoma in situ to invasive breast cancer progression 微rna通过细胞外囊泡优先释放与导管原位癌浸润性乳腺癌进展相关

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-17 DOI: 10.1016/j.canlet.2025.217794

Sugantha Priya Elayapillai , Samrita Dogra , Cole Hladik , James Lausen , Matthew Bruns , Amy Gin Gossett , Fariba Behbod , Chao Xu , Roy Zhang , Wei-Qun Ding , Bethany N. Hannafon

{"title":"Preferential release of microRNAs via extracellular vesicles is associated with ductal carcinoma in situ to invasive breast cancer progression","authors":"Sugantha Priya Elayapillai , Samrita Dogra , Cole Hladik , James Lausen , Matthew Bruns , Amy Gin Gossett , Fariba Behbod , Chao Xu , Roy Zhang , Wei-Qun Ding , Bethany N. Hannafon","doi":"10.1016/j.canlet.2025.217794","DOIUrl":"10.1016/j.canlet.2025.217794","url":null,"abstract":"<div><div>Ductal carcinoma in situ (DCIS) is a precancerous condition that increases the risk of invasive breast cancer (IBC), but not all DCIS cases progress to IBC. The molecular factors driving this transition remain unclear. Small extracellular vesicles (sEVs), or exosomes, play a role in advanced cancer progression, though their function in DCIS is poorly understood. This study explores the role of sEVs and their RNA content in DCIS progression. We found that Rab27A, a key regulator of exosome release, is upregulated in DCIS and IBC tissues compared to normal breast tissue. Inhibiting sEV release by knocking down Rab27A disrupted pro-invasive signaling and reduced invasion in a DCIS mouse model. Using the MCF10 breast cancer progression series, we observed increased microRNA (miRNA) content in sEVs as cells transitioned from normal to malignant, with the most significant differential miRNA expression seen in IBC-derived sEVs. In vivo, DCIS progression raised circulating sEV miRNA levels, which were reduced by Rab27A knockdown. Reintroducing miR-205, enriched in IBC-derived sEVs, suppressed DCIS cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) markers. Co-expression of miR-205 with Rab27A knockdown also suppressed TGF-β signaling, activated MAPK p38, and induced cell cycle arrest and apoptosis. These findings show that the RNA cargo of sEVs changes during malignancy, with specific miRNAs driving DCIS progression. Re-expression of miR-205 offers a promising therapeutic approach to prevent DCIS from becoming invasive.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217794"},"PeriodicalIF":9.1,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101418","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}

引用次数: 0

Corrigendum to “PA28γ acts as a dual regulator of IL-6 and CCL2 and contributes to tumor angiogenesis in oral squamous cell carcinoma” [Cancer Lett. 428 (2018) 192–200] “PA28γ作为IL-6和CCL2的双重调节因子，有助于口腔鳞状细胞癌的肿瘤血管生成”的更正[癌症杂志]. 428 (2018)192-200]

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-17 DOI: 10.1016/j.canlet.2025.217787

Sai Liu , Dongjuan Liu , Xin Zeng , Jiongke Wang , Jiajia Liu , Junxin Cheng , Kexin Lei , Hetian Bai , Ning Ji , Min Zhou , Lu Jiang , Hongxia Dan , Jing Li , Qianming Chen

引用次数: 0

Microbial interactions induce the mutational signature of mismatch repair deficiency in colorectal cancer and associated with EPPK1 mutations 微生物相互作用诱导结直肠癌错配修复缺陷的突变特征并与EPPK1突变相关

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-16 DOI: 10.1016/j.canlet.2025.217807

Dandan Hu , Jialin Zhao , Miaoqing Wu , Ying Zhou , Beile Lyu , Chaoqun Xu , Chao Huang , Zixuan Su , Hui Zhang , Jintao Guo , Weiwei Tang , Gong Chen , Qiyuan Li

{"title":"Microbial interactions induce the mutational signature of mismatch repair deficiency in colorectal cancer and associated with EPPK1 mutations","authors":"Dandan Hu , Jialin Zhao , Miaoqing Wu , Ying Zhou , Beile Lyu , Chaoqun Xu , Chao Huang , Zixuan Su , Hui Zhang , Jintao Guo , Weiwei Tang , Gong Chen , Qiyuan Li","doi":"10.1016/j.canlet.2025.217807","DOIUrl":"10.1016/j.canlet.2025.217807","url":null,"abstract":"<div><div>To better understand the impact of microbial interactions on the clonal evolution of colorectal cancer (CRC), we conducted high-resolution profiling of the gut microbiome of 101 treatment-naïve primary CRC patients using nanopore sequencing. We performed an integrated analysis of microbiome and tumor exome data to identify symbiotic microbes that interactively influence the mutational processes and the subsequent clonality of CRC. Our results suggested that <em>Dialister pneumosintes</em> and <em>Fusobacterium animalis</em> were both associated with somatic <em>EPPK1</em> mutations and promote <strong>SBS6</strong> (mismatch repair deficiency, dMMR) activity. Notably, we showed that the symbiotic architecture of <em>Dialister pneumosintes</em> and <em>Fusobacterium animalis</em> undergoes significant changes with the mutational status of <em>EPPK1</em>. In addition, we identified specific metabolic pathways involving key metabolites that potentially mediate microbial interactions in CRC. These findings provide new insights into the interplay between the gut microbiome and the mutation landscape of colorectal cancer, thereby informing the clonal evolution of CRC and new strategies for precision medicine.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217807"},"PeriodicalIF":9.1,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092863","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}

引用次数: 0