发布求助
文献互助 智能选刊 最新文献

Trends in Cell Biology最新文献

筛选
英文 中文
Tumor-stromal metabolic crosstalk in pancreatic cancer. 胰腺癌的肿瘤-间质代谢串扰。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-26 DOI: 10.1016/j.tcb.2025.04.007
Ravi Thakur, Nicholas J Mullen, Kamiya Mehla, Pankaj K Singh
{"title":"Tumor-stromal metabolic crosstalk in pancreatic cancer.","authors":"Ravi Thakur, Nicholas J Mullen, Kamiya Mehla, Pankaj K Singh","doi":"10.1016/j.tcb.2025.04.007","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.04.007","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a dire prognosis. Standard-of-care chemotherapy regimens offer marginal survival benefit and carry risk of severe toxicity, while immunotherapy approaches have uniformly failed in clinical trials. Extensive desmoplasia in the PDAC tumor microenvironment (TME) disrupts blood flow to and from the tumor, thereby creating a nutrient-depleted, hypoxic, and acidic milieu that suppresses the function of antitumor immune cells and imparts chemotherapy resistance. Additionally, recent seminal studies have demonstrated crucial roles for metabolic crosstalk - the exchange of metabolites between PDAC cells and stromal cell populations in the TME - in establishing and maintaining core malignant behaviors of PDAC: tumor growth, metastasis, immune evasion, and therapy resistance. In this review, we provide a conceptual overview of metabolic crosstalk and how it evolves under various selection pressures in the TME, analyze the landscape of proposed tumorigenic metabolic crosstalk pathways, and highlight potentially druggable nodes.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144163820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Translational control of leukemic metabolism and disease progression. 白血病代谢和疾病进展的翻译控制。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-22 DOI: 10.1016/j.tcb.2025.04.006
François E Mercier, Victor Gife, Raquel Aloyz, Laura Hulea
{"title":"Translational control of leukemic metabolism and disease progression.","authors":"François E Mercier, Victor Gife, Raquel Aloyz, Laura Hulea","doi":"10.1016/j.tcb.2025.04.006","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.04.006","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is an aggressive hematological cancer with a 70% five-year mortality rate. Relapse occurs in approximately half of adults treated with intensive chemotherapy, while responses to targeted therapies are short-lasting. Frequent mutations in signaling pathways, such as FLT3 tyrosine kinase and RAS, lead to dysregulated mammalian target of rapamycin complex 1 (mTORC1)and mitogen-activated protein kinase (MAPK) signaling, increased protein synthesis, enhanced mitochondrial fitness, and metabolic adaptations that drive leukemic cell proliferation and survival. Here, emerging evidence supporting the unique role of eukaryotic initiation factor 4F as a key driver of the expression of proteins regulating leukemic cell metabolism and survival and the potential therapeutic benefit of targeting this pathway pharmacologically in AML are discussed.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144133381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cell cycle regulation by the ribotoxic stress response. 核素毒性应激反应对细胞周期的调控。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-15 DOI: 10.1016/j.tcb.2025.04.005
Connor D McKenney, Sergi Regot
{"title":"Cell cycle regulation by the ribotoxic stress response.","authors":"Connor D McKenney, Sergi Regot","doi":"10.1016/j.tcb.2025.04.005","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.04.005","url":null,"abstract":"<p><p>Cells must sense and respond to numerous stimuli to maintain their function. Stress-activated protein kinases (SAPKs) are part of an integrated network that responds to these stimuli and have critical roles in determining cell behavior. Over the past 5 years, ribosomes and the ribotoxic stress response (RSR) have unexpectedly emerged as critical regulators of the SAPK network and drivers of global cell fate changes. In particular, RSR-SAPK signaling has potent effects on cellular proliferation, with important implications for senescence and cancer. In this review, we discuss cell cycle regulation by the SAPK p38, with a particular focus on how ribotoxic stress affects key cell cycle transitions.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Hypoxia-specific transcriptional condensates drive metastasis. 缺氧特异性转录凝聚物驱动转移。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-15 DOI: 10.1016/j.tcb.2025.04.008
Steven Ingersoll, Xiaojun Ren
{"title":"Hypoxia-specific transcriptional condensates drive metastasis.","authors":"Steven Ingersoll, Xiaojun Ren","doi":"10.1016/j.tcb.2025.04.008","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.04.008","url":null,"abstract":"<p><p>Compartmentalization by phase separation is an emerging principle for regulating transcription. While the compartmentalization mechanisms by which cells regulate genetic activities in response to specific environmental signals remain largely unclear, a recent study by Gao et al. suggests that hypoxia induces the formation of phase-separated condensates, which impacts metastasis-related transcription through chromatin organization.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mitochondrial transfer in endothelial cells and vascular health. 内皮细胞中的线粒体转移与血管健康。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-13 DOI: 10.1016/j.tcb.2025.04.004
Gwang-Bum Im, Juan M Melero-Martin
{"title":"Mitochondrial transfer in endothelial cells and vascular health.","authors":"Gwang-Bum Im, Juan M Melero-Martin","doi":"10.1016/j.tcb.2025.04.004","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.04.004","url":null,"abstract":"<p><p>Mitochondria play a vital role in cellular energy metabolism and vascular health, with their function directly influencing endothelial cell (EC) bioenergetics and integrity. Mitochondrial transfer has emerged as a key mechanism of intercellular communication, impacting angiogenesis, tissue repair, and cellular homeostasis. This review highlights recent findings on mitochondrial transfer, including natural mechanisms - such as tunneling nanotubes (TNTs) and extracellular vesicles (EVs) - and artificial approaches like mitochondrial transplantation. These processes enhance EC function and support vascularization under pathological conditions, including ischemia. While early clinical trials demonstrate therapeutic potential, challenges such as mitochondrial instability and scaling host-derived mitochondria persist. Continued research is essential to optimize mitochondrial transfer and advance its application as a therapeutic strategy for restoring vascular health.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144081916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mapping the funding landscape for public engagement with science. 绘制公众参与科学的资助格局。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-08 DOI: 10.1016/j.tcb.2025.04.001
Fanuel J Muindi
{"title":"Mapping the funding landscape for public engagement with science.","authors":"Fanuel J Muindi","doi":"10.1016/j.tcb.2025.04.001","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.04.001","url":null,"abstract":"<p><p>The funding landscape for public engagement with science (PES) is highly dynamic. More research is needed to better track and understand the rapidly evolving funding landscape in PES. This paper shares insights from an ongoing mapping of the funding landscape and offers recommendations for new research to improve the resolution of such maps.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144051135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The neuronal-like behaviour of macrophages. 巨噬细胞的神经元样行为。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-06 DOI: 10.1016/j.tcb.2025.04.003
Simone Di Giovanni
{"title":"The neuronal-like behaviour of macrophages.","authors":"Simone Di Giovanni","doi":"10.1016/j.tcb.2025.04.003","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.04.003","url":null,"abstract":"<p><p>Tissue-resident macrophages (TRMs) contribute to both organ physiology and pathology by communicating with the nervous system and tissue-resident cells. They have been increasingly reported to be extremely plastic and adaptable, as shown by their broad range of molecular signatures and functional roles well beyond their classical duties as phagocytes. It has recently been found that macrophages can reside in proximity to muscle spindles, which are sensory neurons sensing muscle length. Surprisingly muscle spindle macrophages express neuron-like gene expression signatures and support muscle contraction by releasing glutamate. This behaviour is more in keeping with neurons rather than immune cells. Here, the potential additional roles for muscle spindle macrophages in muscle contraction and locomotion at homeostasis and in disease states will be discussed. It will also be debated whether the use of neurotransmitters by myeloid cells as shared currency to optimise cell to cell communication, to favour neural circuit development, homeostasis and repair is an exception or could rather be the rule.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Extracellular vesicles from the dead: the final message. 来自死者的细胞外囊泡：最后的信息。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-01 Epub Date: 2024-10-21 DOI: 10.1016/j.tcb.2024.09.005
Bo Shi, Thanh Kha Phan, Ivan K H Poon
{"title":"Extracellular vesicles from the dead: the final message.","authors":"Bo Shi, Thanh Kha Phan, Ivan K H Poon","doi":"10.1016/j.tcb.2024.09.005","DOIUrl":"10.1016/j.tcb.2024.09.005","url":null,"abstract":"<p><p>Communication between dying and neighbouring cells is vital to ensure appropriate processes such as tissue repair or inflammation are initiated in response to cell death. As a mechanism to aid intercellular communication, cells undergoing apoptosis can release membrane-bound extracellular vesicles (EVs) called apoptotic-cell-derived EVs (ApoEVs) that can influence downstream processes through biomolecules within or on ApoEVs. ApoEVs are broadly categorised based on size as either large ApoEVs known as apoptotic bodies (ApoBDs) or small ApoEVs (s-ApoEVs). Notably, the mechanisms of ApoBD and s-ApoEV formation are different, and the functions of these two ApoEV subsets are distinct. This Review focuses on the biogenesis and functional properties of both ApoBDs and s-ApoEVs, particularly in the context of cell clearance, cell signalling and disease progression.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"439-452"},"PeriodicalIF":13.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142513569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Emerging roles of ECSIT in immunity and tumorigenesis. ECSIT 在免疫和肿瘤发生中的新作用。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-01 Epub Date: 2024-10-08 DOI: 10.1016/j.tcb.2024.09.003
Shuo Yang, Fiachra Humphries
{"title":"Emerging roles of ECSIT in immunity and tumorigenesis.","authors":"Shuo Yang, Fiachra Humphries","doi":"10.1016/j.tcb.2024.09.003","DOIUrl":"10.1016/j.tcb.2024.09.003","url":null,"abstract":"<p><p>Mitochondria are signaling hubs that produce immunomodulatory metabolites during the immune response. In addition, mitochondria also facilitate the recruitment and anchoring of immune signaling complexes during infection. Evolutionary conserved signaling intermediate in toll (ECSIT) was initially described as a positive regulator of the transcription factor Nuclear factor kappa-light chain enhancer of activated B cells (NF-κB). More recently, ECSIT has emerged as a regulator of bacterial clearance, mitochondrial reactive oxygen species (mROS), and mitophagy. In addition, ECSIT has been identified as a control point in responding to viral infection and tumorigenesis. Notably, ECSIT loss in different models and cell types has been found to lead to enhanced tumorigenesis. Thus, ECSIT functions as a metabolic tumor suppressor and limits cancer pathogenesis. In this review, we highlight the key functions and crosstalk mechanisms that ECSIT bridges between cell metabolism and immunity and focus then on the antitumor role of ECSIT independent of immunity.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"426-438"},"PeriodicalIF":13.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
When RNA damage induces DNA breaks. 当RNA损伤导致DNA断裂。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2025-05-01 Epub Date: 2025-04-09 DOI: 10.1016/j.tcb.2025.03.004
Ivan Mikicic, Petra Beli
{"title":"When RNA damage induces DNA breaks.","authors":"Ivan Mikicic, Petra Beli","doi":"10.1016/j.tcb.2025.03.004","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.03.004","url":null,"abstract":"<p><p>While alkylated mRNAs are known to activate ribosome quality control in the cytoplasm, how do cells deal with damaged RNAs in the nucleus? In their current work, Tsao et al. discover a new pathway of RNA damage repair and unexpectedly find that RNA alkylation can induce R-loops and DNA breaks.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":"35 5","pages":"359-360"},"PeriodicalIF":13.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
下一页 尾页
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整，为了账户安全，请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们：info@booksci.cn Book学术提供免费学术资源搜索服务，方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号：481959085
Book学术官方微信