Life sciences最新文献

{"title":"FUT3 promotes gastric cancer cell migration by synthesizing Lea on ITGA6 and GLG1, affecting adhesion and vesicle distribution","authors":"Fei Wu ,&nbsp;Li Cao ,&nbsp;Jinyuan Zhang ,&nbsp;Shuang Cai ,&nbsp;Huizi Wu ,&nbsp;Jiyu Miao ,&nbsp;Lingyu Zhao ,&nbsp;Changan Zhao ,&nbsp;Xiaofei Wang ,&nbsp;Muhammad Anas Ramzan ,&nbsp;Sadiq Ali ,&nbsp;Feng Wu ,&nbsp;Lei Ni ,&nbsp;Liying Liu ,&nbsp;Yannan Qin ,&nbsp;Chen Huang","doi":"10.1016/j.lfs.2024.123193","DOIUrl":"10.1016/j.lfs.2024.123193","url":null,"abstract":"<div><h3>Aims</h3><div>Lewis antigen plays an important role in the progression of gastric cancer (GC), FUT3 is a key enzyme in the synthesis of Lewis antigen, but the molecular mechanism of its promotion of GC progression remains unclear.</div></div><div><h3>Main methods</h3><div>We used Lea-antibody capturing coupled with mass spectrometry to identify the target proteins of FUT3, immunofluorescence (IF), molecular biology and cell function experiments were conducted to clarify the molecular mechanism of FUT3 promoting the migration and invasion of GC cells by regulating Lea glycosylation on ITGA6 and GLG1.</div></div><div><h3>Key findings</h3><div>FUT3 promote migration and invasion of GC cells. FUT3 silencing in GC cells led to the aggregation of integrin α6β4 on the plasma membrane, associated with focal adhesion and hemidesmosome, and decreased GLG1 distribution in cellular vesicles. IGP analysis revealed Lea structure in 10 N-glycans of 2 glycosites for ITGA6 and 31 N-glycans of 4 glycosites for GLG1. Silencing ITGA6 promoted migration and invasion, while silencing GLG1 inhibited these processes in GC cells, regulated by FUT3-mediated Lea synthesis.</div></div><div><h3>Significance</h3><div>In conclusion, FUT3's promotion of GC cell migration and invasion is attributed to Lea synthesis on ITGA6, impacting cell adhesion, and on GLG1, influencing distribution in intracellular vesicles. These findings may contribute to developing novel therapeutic targets for inhibiting or controlling the metastatic behavior of GC cells and enhancing our understanding of Lea's role in regulating protein functions.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"359 ","pages":"Article 123193"},"PeriodicalIF":5.2,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vaping/e-cigarette-induced pulmonary extracellular vesicles contribute to exacerbated cardiomyocyte impairment through the translocation of ERK5","authors":"Caihong Liu ,&nbsp;Yanwei Zhang ,&nbsp;Jianli Zhao ,&nbsp;John Zhang ,&nbsp;Zhijun Meng ,&nbsp;Yuhui Yang ,&nbsp;Yaoli Xie ,&nbsp;Xiangying Jiao ,&nbsp;Bin Liang ,&nbsp;Jimin Cao ,&nbsp;Yajing Wang","doi":"10.1016/j.lfs.2024.123195","DOIUrl":"10.1016/j.lfs.2024.123195","url":null,"abstract":"<div><h3>Aims</h3><div>The impact of e-cigarettes/vaping on cardiac function remains contradictory owing to insufficient direct evidence of interorgan communication. Extracellular vesicles (EVs) have protective or detrimental effects depending on pathological conditions, making it crucial to understand their role in lung-cardiac cell interactions mediated by vaping inhalation.</div></div><div><h3>Methods and key findings</h3><div>Pulmonary EVs were characterized from animals that underwent 12 weeks of nicotine inhalation (vaping component) (EVs^Nicotine) or vehicle control (EVs^Vehicle). EVs^Nicotine significantly increased in size and abundance compared with EVs^Vehicle. The direct effect of EVs ^Nicotine and EVs ^Vehicle on cardiomyocytes was then assessed in vitro and in vivo. EVs ^Nicotine led to a decrease in cardiac function as manifested by reduced cardiac contractility and impaired relaxation. EVs ^Nicotine induced increased levels of cleaved caspase-1 and cleaved caspase-11 in cardiomyocytes, indicating the promotion of pyroptosis. Meanwhile, EVs^Nicotine stimulated the secretion of fibrotic factors. Further analysis revealed that nicotine inhalation stimulated EVs ^Nicotine enriched with high levels of ERK5 (EVs ^Nicotine-ERK5). It was discovered that these EVs derived from pulmonary epithelial cells. Furthermore, inhibiting cardiac ERK5 blunted the EVs ^Nicotine-induced pyroptosis and fibrotic factor secretion. We further identified GATA4, a pro-pyroptosis transcription factor, as being activated through ERK5-dependent phosphorylation.</div></div><div><h3>Significance</h3><div>Our research demonstrates that nicotine inhalation exacerbates cardiac injury through the activation of EVs derived from the lungs during e-cigarettes/vaping. Specifically, the EVs containing ERK5 play a crucial role in mediating the detrimental effects on cardiac function. This research provides new insights into the cardiac toxicity of vaping and highlights the role of EVs ^Nicotine-ERK5 in this process.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"358 ","pages":"Article 123195"},"PeriodicalIF":5.2,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRF1-induced mmu_circ_0001388/hsa_circ_0029470 confers ferroptosis resistance in ischemic acute kidney injury via the miR-193b-3p/TCF4/GPX4 axis","authors":"Qiang Zheng ,&nbsp;Dongshan Zhang ,&nbsp;Jihong Xing","doi":"10.1016/j.lfs.2024.123190","DOIUrl":"10.1016/j.lfs.2024.123190","url":null,"abstract":"<div><h3>Aims</h3><div>Circular RNAs (circRNAs) are critical in the progression of ischemic acute kidney injury (AKI). Nevertheless, the specific functions and regulatory pathways of mmu_circ_0001388 and hsa_circ_0029470 remain elusive.</div></div><div><h3>Methods</h3><div>Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to assess the expression patterns of mmu_circ_0001388, hsa_circ_0029470, and miR-139b-3p. Protein expressions of nuclear respiratory factor 1 (NRF1), transcription factor 4 (TCF4), glutathione peroxidase 4 (GPX4), and Acyl-CoA synthetase long-chain family member 4 (ACSL4) were identified via immunoblotting. Furthermore, the functions and control mechanisms of mmu_circ_003062 and hsa_circ_0075663 were examined via diverse cell and animal studies, encompassing bioinformatics prediction, dual-luciferase reporter (DLR), chromatin immunoprecipitation (ChIP), fluorescence in situ hybridization (FISH), flow cytometry (FCM), hematoxylin and eosin (H&amp;E) staining, dihydroethidium (DHE), TUNEL, immunohistochemistry, and transmission electron microscopy (TEM), and Fe²⁺ assay.</div></div><div><h3>Key findings</h3><div>Initially, the induction of mmu_circ_0001388 by NRF1 was observed in vitro and in vivo following ischemia/reperfusion (I/R) injury. Subsequently, knockdown or overexpression of mmu_circ_0001388 was found to either promote or inhibit ferroptosis caused by I/R in Boston University mouse proximal tubule (BUMPT) cells, respectively. From a mechanistic standpoint, mmu_circ_0001388 was found to function as a sponge for miR-193b-3p, which promoted TCF4 and subsequently enhanced GPX4, thereby suppressing ferroptosis. Finally, the overexpression of mmu_circ_0001388 was shown to ameliorate I/R-induced AKI in mice. In parallel, hsa_circ_0029470, homologous to mmu_circ_0001388, demonstrated an identical control pathway in human renal tubular epithelial (HK-2) cells.</div></div><div><h3>Significance</h3><div>The NRF1/mmu_circ_0001388, hsa_circ_0029470/miR-193b-3p/TCF4/GPX4 axis is pivotal in regulating ferroptosis induced by ischemic AKI and holds potential as a therapeutic target.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"358 ","pages":"Article 123190"},"PeriodicalIF":5.2,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Indole-3-acetic acid attenuates pulmonary fibrosis by modulating lung microbiota, inhibiting fibroblast activation, and alleviating alveolar epithelial cell senescence","authors":"Jinzhong Zhuo ,&nbsp;Dongyu Liu ,&nbsp;Qi Yu ,&nbsp;Minxuan Hu ,&nbsp;Haohua Huang ,&nbsp;Yixin Chen ,&nbsp;Yanqun Li ,&nbsp;Yimei Gao ,&nbsp;Weimou Chen ,&nbsp;Xiaojin Meng ,&nbsp;Fei Zou ,&nbsp;Jinming Zhang ,&nbsp;Shaoxi Cai ,&nbsp;Hangming Dong","doi":"10.1016/j.lfs.2024.123191","DOIUrl":"10.1016/j.lfs.2024.123191","url":null,"abstract":"<div><h3>Aim</h3><div>Pulmonary fibrosis (PF) is a relentlessly progressive disorder characterized by high mortality and limited effective therapeutic options. Indole-3-acetic acid (IAA), originally recognized as a plant hormone, is also identified as a tryptophan-derived metabolite catabolized from microbiota in mammals. IAA has exhibited antioxidative, anti-inflammatory, and anti-tumor effects in various disorders, yet its role in PF remains elusive.</div></div><div><h3>Main methods</h3><div>Bleomycin (BLM) was employed to induce PF in a mouse model. TGF-β1 was utilized in primary mouse lung fibroblasts (pMLFs) to establish a pro-fibrotic in vitro cellular model, and in A549 cells to create an in vitro cellular senescence model. The therapeutic effects of IAA on PF were evaluated using hematoxylin-eosin staining, immunofluorescence staining, western blotting, SA-β-gal assay, and network pharmacology analysis. Additionally, the effect of IAA on lung microbiota of PF was investigated using 16S rRNA gene sequencing analysis.</div></div><div><h3>Key findings</h3><div>we observed a significant reduction in IAA levels in both PF patients and mouse models. Moreover, we demonstrated the therapeutic potential of IAA in alleviating PF in BLM-induced mouse models, showing a dose-dependent response. Mechanistically, we delineated three perspectives. Firstly, IAA promoted autophagic flux by inhibiting the PI3K/AKT/mTOR pathway, thereby suppressing lung fibroblast differentiation and extracellular matrix (ECM) deposition. Secondly, IAA attenuated alveolar epithelial cell senescence by modulating the PI3K/AKT and HIF-1 pathways. Lastly, IAA displayed the ability to mitigate PF by modulating the structure and composition of lung microbiota.</div></div><div><h3>Significance</h3><div>Our study demonstrates that IAA alleviates PF through multiple pathways, highlighting its potential as a therapeutic agent.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"359 ","pages":"Article 123191"},"PeriodicalIF":5.2,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytological changes in radiation-induced lung injury","authors":"Yun Wang,&nbsp;Jianghong Zhang,&nbsp;Chunlin Shao","doi":"10.1016/j.lfs.2024.123188","DOIUrl":"10.1016/j.lfs.2024.123188","url":null,"abstract":"<div><div>Radiation-induced lung injury (RILI) is a prevalent complication associated with radiotherapy for thoracic tumors. Based on the pathological progression, it can be categorized into two stages: early radiation pneumonitis and late radiation pulmonary fibrosis. The occurrence of RILI not only constrains the therapeutic dose that can be administered to the tumor target area but also significantly impairs patients' health and quality of life, thereby limiting the efficacy and applicability of radiotherapy. To effectively prevent and mitigate the development of RILI, it is crucial to disclose its underlying mechanisms. This review aims to elucidate the specific mechanisms involved in RILI and to examine the roles of various cell types, including lung parenchymal cells and different immune cells. The functions and interactions of lung epithelial cells, pulmonary vascular endothelial cells, a variety of immune cells, and fibroblasts during different stages of inflammation, tissue repair, and fibrosis following radiation-induced lung injury are analyzed. A comprehensive understanding of the dynamic changes in these cellular components is anticipated to offer new strategies for the prevention of RILI.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"358 ","pages":"Article 123188"},"PeriodicalIF":5.2,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multicellular tumor spheroids: A convenient in vitro model for translational cancer research","authors":"Tushar Patel ,&nbsp;Neeraj Jain","doi":"10.1016/j.lfs.2024.123184","DOIUrl":"10.1016/j.lfs.2024.123184","url":null,"abstract":"<div><div>In the attempts to mitigate uncertainties in the results of monolayer culture for the identification of cancer therapeutic targets and compounds, there has been a growing interest in using 3D cancer spheroid models, which include tumorospheres (TSs), tissue-derived tumor spheres (TDTSs), organotypic multicellular tumor spheroids (OMSs), and multicellular tumor spheroids (MCTSs). The MCTSs, either Mono-MCTSs or Hetero-MCTSs, with or without scaffold, in particular, offer numerous advantages over other spheroid models, including easy cultivation, high reproducibility, accessibility, high throughput, controllable size, well-rounded shape, simplicity of genetic manipulation, economical and availability of various biological methods for their development. In this review, we have attempted to discuss the role of MCTSs concerning various aspects of translational cancer research, such as drug response and penetration, cell-cell interaction, and invasion and metastasis. However, the Mono-MCTSs, either scaffold-free or scaffold-based, may not adequately represent the cellular heterogeneity and complexity of clinical tumors, limiting their utility in translational cancer research. Conversely, Hetero-MCTS models, both scaffold-free and scaffold-based, show better suitability due to the presence of a similar in vivo type tumor microenvironment. Nonetheless, scaffold-based Hetero-MCTS models show batch variability and challenges in performing quantitative assays due to difficulties extracting spheroids and cells from scaffolds. Further, incorporating stromal cells with cancer cells in a more precise ratio to develop Hetero-MCTSs can enhance the model's relevance, yielding more clinically reliable outcomes for drug candidates and improving insights into tumor biology.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"358 ","pages":"Article 123184"},"PeriodicalIF":5.2,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The roles of extracellular vesicles in gliomas: Challenge or opportunity?","authors":"Le Huang ,&nbsp;Jianhao Zhan ,&nbsp;Yao Li ,&nbsp;Kai Huang ,&nbsp;Xingen Zhu ,&nbsp;Jingying Li","doi":"10.1016/j.lfs.2024.123150","DOIUrl":"10.1016/j.lfs.2024.123150","url":null,"abstract":"<div><div>Gliomas are increasingly becoming a major disease affecting human health, and current treatments are not as effective as expected. Deeper insights into glioma heterogeneity and the search for new diagnostic and therapeutic strategies appear to be urgent. Gliomas adapt to their surroundings and form a supportive tumor microenvironment (TME). Glioma cells will communicate with the surrounding cells through extracellular vesicles (EVs) carrying bioactive substances such as nucleic acids, proteins and lipids which is related to the modification to various metabolic pathways and regulation of biological behaviors, and this regulation can be bidirectional, widely existing between cells in the TME, constituting a complex network of interactions. This complex regulation can affect glioma therapy, leading to different types of resistance. Because of the feasibility of EVs isolation in various body fluids, they have a promising usage in the diagnosis and monitoring of gliomas. At the same time, the nature of EVs to cross the blood-brain barrier (BBB) confers potential for their use as drug delivery systems. In this review, we will focus on the roles and functions of EVs derived from different cellular origins in the glioma microenvironment and the intercellular regulatory networks, and explore possible clinical applications in glioma diagnosis and precision therapy.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"358 ","pages":"Article 123150"},"PeriodicalIF":5.2,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precision medicine advances in cystic fibrosis: Exploring genetic pathways for targeted therapies","authors":"Abinesh R.S.,&nbsp;Madhav R.,&nbsp;K. Trideva Sastri,&nbsp;Meghana G.S.,&nbsp;Akhila A.R.,&nbsp;Balamuralidhara V.","doi":"10.1016/j.lfs.2024.123186","DOIUrl":"10.1016/j.lfs.2024.123186","url":null,"abstract":"<div><div>Personalized medicine has transformed the treatment of cystic fibrosis (CF), providing customized therapeutic approaches based on individual genetic profiles. This review explores the genetic foundations of CF, focusing on mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene and their implications for the development of the disease. The advent of genetic testing has enabled the association of specific mutations to disease severity, leading to the development of CFTR modulators like Ivacaftor, Lumacaftor, and Tezacaftor. Beyond CFTR mutations, genetic modifiers, including gene replacement therapy, genetic manipulation, lentivirus, and non-viral gene therapy formulations, along with environmental factors, play critical roles in influencing disease expression and outcomes. The identification of these modifiers is essential for optimizing therapeutic strategies. Emerging biomarkers, including inflammatory markers and pulmonary function indicators, aid in early disease detection and monitoring progression. Omics technologies are uncovering novel biomarkers, enabling more precise disease management.</div><div>Pharmacogenomics has become integral to CF care, allowing for personalized approaches that consider genetic variations influencing drug metabolism, especially in antibiotics and anti-inflammatory therapies. The future of CF treatment lies in precision therapies, including CFTR modulators and cutting-edge techniques like gene therapy and CRISPR-Cas9 for mutation correction. As research evolves, these advances can improve patient outcomes while minimizing adverse effects. Ethical considerations and regulatory challenges remain critical as personalized medicine advances, ensuring equitable access and the long-term effectiveness of these innovative therapies.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"358 ","pages":"Article 123186"},"PeriodicalIF":5.2,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of orofacial pain potentiates fibromyalgia symptoms in mice: Relevance of nociceptin system","authors":"Maria C.C. Volkweis ,&nbsp;Luisa A. Tomasi ,&nbsp;Gabriella C. Santos ,&nbsp;Ana P.A. Dagnino ,&nbsp;Marina Estrázulas ,&nbsp;Maria M. Campos","doi":"10.1016/j.lfs.2024.123183","DOIUrl":"10.1016/j.lfs.2024.123183","url":null,"abstract":"<div><h3>Aims</h3><div>Fibromyalgia patients might experience temporomandibular disorder (TMD) as a comorbidity. However, the connection between these two syndromes is not fully understood. Nociceptin (N/OFQ) and NOP receptors are implicated in both conditions, but their relevance in the comorbidity needs investigation. This study featured a comorbidity model of fibromyalgia plus TMD in mice, attempting to evaluate the significance of the N/OFQ-NOP receptor in this paradigm.</div></div><div><h3>Materials and methods</h3><div>Female CF-1 mice were submitted to the fibromyalgia model induced by three daily consecutive injections of reserpine (0.25 mg/kg) and received an intra-masseter injection of complete Freund's adjuvant (CFA; 10 μl; diluted 1:1) on day four.</div></div><div><h3>Key findings</h3><div>There was a rise in nocifensive and depression-like behaviors in the comorbidity group, as evaluated by the Grimace scores and the tail suspension test (TST). This group displayed anxiogenic-like effects in the hole board and the elevated plus maze tests. The comorbidity group showed an increment of c-Fos immunopositivity in the ipsilateral side of CFA injection, in the trigeminal ganglion (TG) and thalamus. The administration of N/OFQ (1 nmol/kg, i.p.) boosted the Grimace scores in the comorbidity group, with no effect for the NOP receptor antagonist UFP-101 (1 nmol/kg, i.p.). Either NOP ligand failed to alter depression or anxiety behavioral changes. Alternatively, pregabalin (30 mg/kg; i.p.) reduced the nociceptive responses and the number of head dips in the hole board.</div></div><div><h3>Significance</h3><div>Data reveal new evidence suggesting that inducing TMD with CFA may worsen fibromyalgia symptoms in reserpine-treated mice, an effect partially regulated by systemic N/OFQ.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"358 ","pages":"Article 123183"},"PeriodicalIF":5.2,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechano-assisted strategies to improve cancer chemotherapy","authors":"Shanshan Zhu ,&nbsp;Guorui Jin ,&nbsp;Xiaocong He ,&nbsp;Yuan Li ,&nbsp;Feng Xu ,&nbsp;Hui Guo","doi":"10.1016/j.lfs.2024.123178","DOIUrl":"10.1016/j.lfs.2024.123178","url":null,"abstract":"<div><div>Chemotherapy remains a cornerstone in cancer treatment; however, its effectiveness is frequently undermined by the development of drug resistance. Recent studies underscores the pivotal role of the tumor mechanical microenvironment (TMME) and the emerging field of mechanical nanomedicine in tackling chemo-resistance. This review offers an in-depth analysis of mechano-assisted strategies aimed at mitigating chemo-resistance through the modification of the TMME and the refinement of mechanical nanomedicine delivery systems. We explore the potential of targeting abnormal tumor mechanical properties as a promising avenue for enhancing the efficacy of cancer chemotherapy, which offers novel directions for advancing future cancer therapies, especially from the mechanomedicine perspective.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"359 ","pages":"Article 123178"},"PeriodicalIF":5.2,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}