Pub Date : 2025-07-04DOI: 10.1016/j.pbiomolbio.2025.07.001
Xingkai Wang , Kunpeng Zhu , Jianping Hu , Chunlin Zhang
Osteosarcoma represents the greatest percentage of malignant tumors in the bone and is distinguished by its high incidence of aggressiveness, metastasis, and recurrence after therapy. At present, the treatment strategies for osteosarcoma typically encompass surgical resection, chemotherapy, targeted therapy, and radiotherapy. Even though there are now more extensive treatment options for osteosarcoma, the prognosis is still dismal, particularly for those who have metastatic osteosarcoma. Developing efficient treatment approaches therefore becomes crucial to turning things around. With the ongoing advancements in science and technology, together with the integration of research in diverse domains, more creative approaches to treating osteosarcoma have been explored in recent years. This article reviews the cutting-edge advances in osteosarcoma immunotherapy, biomedical materials, and gut microbiota in the field of osteosarcoma treatment. Ultimately, our goal is to increase the overall survival rate for patients with osteosarcoma by providing robust theoretical support for the development of innovative medications through an in-depth analysis and summary of the most recent advancements and obstacles facing osteosarcoma treatment.
{"title":"Advances and challenges in the treatment of osteosarcoma","authors":"Xingkai Wang , Kunpeng Zhu , Jianping Hu , Chunlin Zhang","doi":"10.1016/j.pbiomolbio.2025.07.001","DOIUrl":"10.1016/j.pbiomolbio.2025.07.001","url":null,"abstract":"<div><div>Osteosarcoma represents the greatest percentage of malignant tumors in the bone and is distinguished by its high incidence of aggressiveness, metastasis, and recurrence after therapy. At present, the treatment strategies for osteosarcoma typically encompass surgical resection, chemotherapy, targeted therapy, and radiotherapy. Even though there are now more extensive treatment options for osteosarcoma, the prognosis is still dismal, particularly for those who have metastatic osteosarcoma. Developing efficient treatment approaches therefore becomes crucial to turning things around. With the ongoing advancements in science and technology, together with the integration of research in diverse domains, more creative approaches to treating osteosarcoma have been explored in recent years. This article reviews the cutting-edge advances in osteosarcoma immunotherapy, biomedical materials, and gut microbiota in the field of osteosarcoma treatment. Ultimately, our goal is to increase the overall survival rate for patients with osteosarcoma by providing robust theoretical support for the development of innovative medications through an in-depth analysis and summary of the most recent advancements and obstacles facing osteosarcoma treatment.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Pages 60-74"},"PeriodicalIF":3.2,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144576926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-25DOI: 10.1016/j.pbiomolbio.2025.06.001
Jingpeng Guo , Wenxing Jia , Shengnan Jia
Sialylation is a critical glycosylation process involving the covalent attachment of sialic acid residues to the terminal glycans of glycoproteins and glycolipids. This modification is predominantly mediated by sialyltransferases (STs), which play pivotal roles in cell signaling, immune response, and cellular adhesion and migration. Aberrant sialylation, resulting from dysregulated expression of STs, is a hallmark of cancer, frequently observed on the surfaces of both tumor and stromal cells. The ST3GAL family, a key subset of STs, facilitates α-2,3-sialylation and has emerged as a crucial regulator of tumor cell proliferation, motility, drug resistance, and the immunosuppressive tumor microenvironment. Despite its recognized significance, a comprehensive synthesis of the diverse roles and molecular mechanisms of the ST3GAL family in tumor progression is still lacking. This review consolidates current knowledge on the molecular structure, biological functions, and pathological implications of the ST3GAL family in cancer, with a focus on its roles in signal modulation, immune evasion, and therapeutic targeting. By highlighting its potential as a key player in oncogenic processes, this review aims to provide novel insights to inform future research and clinical applications.
{"title":"The multifaceted roles of ST3GAL family in cancer: Mechanistic insights and therapeutic implications","authors":"Jingpeng Guo , Wenxing Jia , Shengnan Jia","doi":"10.1016/j.pbiomolbio.2025.06.001","DOIUrl":"10.1016/j.pbiomolbio.2025.06.001","url":null,"abstract":"<div><div>Sialylation is a critical glycosylation process involving the covalent attachment of sialic acid residues to the terminal glycans of glycoproteins and glycolipids. This modification is predominantly mediated by sialyltransferases (STs), which play pivotal roles in cell signaling, immune response, and cellular adhesion and migration. Aberrant sialylation, resulting from dysregulated expression of STs, is a hallmark of cancer, frequently observed on the surfaces of both tumor and stromal cells. The ST3GAL family, a key subset of STs, facilitates α-2,3-sialylation and has emerged as a crucial regulator of tumor cell proliferation, motility, drug resistance, and the immunosuppressive tumor microenvironment. Despite its recognized significance, a comprehensive synthesis of the diverse roles and molecular mechanisms of the ST3GAL family in tumor progression is still lacking. This review consolidates current knowledge on the molecular structure, biological functions, and pathological implications of the ST3GAL family in cancer, with a focus on its roles in signal modulation, immune evasion, and therapeutic targeting. By highlighting its potential as a key player in oncogenic processes, this review aims to provide novel insights to inform future research and clinical applications.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Pages 48-59"},"PeriodicalIF":3.2,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-18DOI: 10.1016/j.pbiomolbio.2025.06.002
Yang He , Jian Lin , Yi Li , Weixing Zeng , Yongsheng Li
Background
Venous malformations (VMs) are common vascular anomalies characterized by abnormal endothelial cell proliferation, a paucity of vascular wall cells, and irregular vascular structures. While pathogenic gene mutations are the genetic basis of VMs, the cellular heterogeneity, tissue specificity, and underlying mechanisms remain poorly understood. VMs are increasingly recognized as vascular anomalies with tumor-like mechanisms, highlighting the critical roles of cellular heterogeneity and tissue specificity in pathogenesis.
Methods
This review systematically examines recent advances in VMs research, focusing on cellular heterogeneity and tissue specificity. It summarizes key mutated genes, the roles of various cell types, and their interactions within lesions. By comparing physiological differences between arteries and veins, we explore the tissue-specific origins of VMs. Additionally, we evaluate current cellular and animal models, discussing their strengths and limitations in simulating pathological features, including cellular heterogeneity and tissue specificity.
Results
The development of VMs is strongly linked to genetic mutations in endothelial cells, as well as functional alterations in endothelial progenitor cells, vascular wall cells, and other perivascular cells. Lesion tissues exhibit significant heterogeneity in cell function, gene/protein expression, and signal transduction. Tissue specificity is influenced by differences in environmental factors, tissue structure, and gene expression between arteries and veins, explaining why VMs predominantly affect veins.
Conclusions
VMs development involves interactions among pathogenic gene mutations, cellular heterogeneity, and tissue specificity. Understanding these mechanisms will elucidate VMs pathogenesis and inform precision therapies. Future research should focus on cell-type interactions, the role of tissue specificity in disease progression, and developing targeted therapeutic strategies.
{"title":"Cellular heterogeneity and tissue specificity in venous malformations: Implications for pathogenesis and targeted therapies","authors":"Yang He , Jian Lin , Yi Li , Weixing Zeng , Yongsheng Li","doi":"10.1016/j.pbiomolbio.2025.06.002","DOIUrl":"10.1016/j.pbiomolbio.2025.06.002","url":null,"abstract":"<div><h3>Background</h3><div>Venous malformations (VMs) are common vascular anomalies characterized by abnormal endothelial cell proliferation, a paucity of vascular wall cells, and irregular vascular structures. While pathogenic gene mutations are the genetic basis of VMs, the cellular heterogeneity, tissue specificity, and underlying mechanisms remain poorly understood. VMs are increasingly recognized as vascular anomalies with tumor-like mechanisms, highlighting the critical roles of cellular heterogeneity and tissue specificity in pathogenesis.</div></div><div><h3>Methods</h3><div>This review systematically examines recent advances in VMs research, focusing on cellular heterogeneity and tissue specificity. It summarizes key mutated genes, the roles of various cell types, and their interactions within lesions. By comparing physiological differences between arteries and veins, we explore the tissue-specific origins of VMs. Additionally, we evaluate current cellular and animal models, discussing their strengths and limitations in simulating pathological features, including cellular heterogeneity and tissue specificity.</div></div><div><h3>Results</h3><div>The development of VMs is strongly linked to genetic mutations in endothelial cells, as well as functional alterations in endothelial progenitor cells, vascular wall cells, and other perivascular cells. Lesion tissues exhibit significant heterogeneity in cell function, gene/protein expression, and signal transduction. Tissue specificity is influenced by differences in environmental factors, tissue structure, and gene expression between arteries and veins, explaining why VMs predominantly affect veins.</div></div><div><h3>Conclusions</h3><div>VMs development involves interactions among pathogenic gene mutations, cellular heterogeneity, and tissue specificity. Understanding these mechanisms will elucidate VMs pathogenesis and inform precision therapies. Future research should focus on cell-type interactions, the role of tissue specificity in disease progression, and developing targeted therapeutic strategies.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Pages 34-47"},"PeriodicalIF":3.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144335985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-02DOI: 10.1016/j.pbiomolbio.2025.05.004
Baiyan Wang , Jiayi Li , Dandan Guo , Shuxuan Li , Yalan Li , Qianqian Wang , Yi Yang , Wei Chen , Shuying Feng
Cancer diagnosis and treatment remains challenging, with unresolved issues such as low targeting, drug resistance, and numerous adverse reactions from chemotherapy. Cell membrane biomimetic modified nanoparticles(CMBMNPs), wrapping cell membrane on nanoparticles can achieve homologous cell mimicry, so that it can obtain the functions and properties of the type of cell, with strong targeting ability, strong immune evasion ability, long in vivo circulation time, etc., which is getting more and more attention. This article describes the preparation process of CMBMNPs and the different clinical effects of different types of nanoparticles and mimicking cell membranes in order to select the right match for use. In addition, we list in detail several important features of CMBMNPs as well as the advantages of CMBMNPs in areas related to cancer diagnosis and therapy, and look forward to the future challenges and prospects of cell membrane-generating nanotechnology, which provides new insights into the application of CMBMNPs in cancer diagnosis and therapy.
{"title":"The application progress of cell membrane biomimetic nanoparticles in cancer diagnosis and treatment1","authors":"Baiyan Wang , Jiayi Li , Dandan Guo , Shuxuan Li , Yalan Li , Qianqian Wang , Yi Yang , Wei Chen , Shuying Feng","doi":"10.1016/j.pbiomolbio.2025.05.004","DOIUrl":"10.1016/j.pbiomolbio.2025.05.004","url":null,"abstract":"<div><div>Cancer diagnosis and treatment remains challenging, with unresolved issues such as low targeting, drug resistance, and numerous adverse reactions from chemotherapy. Cell membrane biomimetic modified nanoparticles(CMBMNPs), wrapping cell membrane on nanoparticles can achieve homologous cell mimicry, so that it can obtain the functions and properties of the type of cell, with strong targeting ability, strong immune evasion ability, long in vivo circulation time, etc., which is getting more and more attention. This article describes the preparation process of CMBMNPs and the different clinical effects of different types of nanoparticles and mimicking cell membranes in order to select the right match for use. In addition, we list in detail several important features of CMBMNPs as well as the advantages of CMBMNPs in areas related to cancer diagnosis and therapy, and look forward to the future challenges and prospects of cell membrane-generating nanotechnology, which provides new insights into the application of CMBMNPs in cancer diagnosis and therapy.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Pages 21-33"},"PeriodicalIF":3.2,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-15DOI: 10.1016/j.pbiomolbio.2025.05.002
Jing Quan , Chunhong Zhang , Xue Chen , Xinfei Cai , Xiangjian Luo
Lipid droplets (LDs) store lipids in cells, provide phospholipids for membrane synthesis, and maintain the intracellular balance of energy and lipid metabolism. Undoubtedly, the crosstalk between LDs and other organelles is the foundation for performing functions. Many studies indicate that LDs promote tumor progression. LD accumulation has been observed in a variety of cancers, and high LD content is associated with malignant phenotype and poor prognosis of cancers. In this paper, we summarized the intimate crosstalk between LDs and intracellular organelles, including endoplasmic reticulum (ER), mitochondria, lysosomes and peroxisomes, and addressed the effects of LD-organelle crosstalk on cancer initiation and progression. We also integrated the changes of LD-organelle interactions in cancers to provide an insightful knowledge for cancer therapeutics.
{"title":"Lipid droplet - organelle crosstalk and its implication in cancer","authors":"Jing Quan , Chunhong Zhang , Xue Chen , Xinfei Cai , Xiangjian Luo","doi":"10.1016/j.pbiomolbio.2025.05.002","DOIUrl":"10.1016/j.pbiomolbio.2025.05.002","url":null,"abstract":"<div><div>Lipid droplets (LDs) store lipids in cells, provide phospholipids for membrane synthesis, and maintain the intracellular balance of energy and lipid metabolism. Undoubtedly, the crosstalk between LDs and other organelles is the foundation for performing functions. Many studies indicate that LDs promote tumor progression. LD accumulation has been observed in a variety of cancers, and high LD content is associated with malignant phenotype and poor prognosis of cancers. In this paper, we summarized the intimate crosstalk between LDs and intracellular organelles, including endoplasmic reticulum (ER), mitochondria, lysosomes and peroxisomes, and addressed the effects of LD-organelle crosstalk on cancer initiation and progression. We also integrated the changes of LD-organelle interactions in cancers to provide an insightful knowledge for cancer therapeutics.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Pages 11-20"},"PeriodicalIF":3.2,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144095738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-13DOI: 10.1016/j.pbiomolbio.2025.05.003
Yu Zeng , Yonggang Tao , Guotu Du , Tianyu Huang , Shicheng Chen , Longmei Fan , Neng Zhang
Metabolic reprogramming, a hallmark of malignancy, enables tumor cells to adapt to the harsh and dynamic tumor microenvironment (TME) by altering metabolic pathways. Hypoxia, prevalent in solid tumors, activates hypoxia inducible factor 1α (HIF-1α). HIF-1α drives metabolic reprogramming, enhancing glycolysis primarily through the Warburg effect to reduce oxygen dependence and facilitate tumor cell growth/proliferation. The above process is associated with accelerated tumor cell dedifferentiation and enhanced stemness, generating cancer stem cells (CSCs) which possesses the potential for self-renewal and differentiation that can differentiate into a wide range of subtypes of tumor cells and fuel tumor heterogeneity, metastasis, and recurrence, complicating therapy. This review examines the HIF-1α-glycolysis-dedifferentiation crosstalk mechanisms, expecting that indirect inhibition of HIF-1α by targeting metabolic enzymes, metabolites, or their signaling pathways will offer an effective therapeutic strategy to improve the cancer treatment outcomes.
{"title":"Advances in the mechanisms of HIF-1α-enhanced tumor glycolysis and its relation to dedifferentiation","authors":"Yu Zeng , Yonggang Tao , Guotu Du , Tianyu Huang , Shicheng Chen , Longmei Fan , Neng Zhang","doi":"10.1016/j.pbiomolbio.2025.05.003","DOIUrl":"10.1016/j.pbiomolbio.2025.05.003","url":null,"abstract":"<div><div>Metabolic reprogramming, a hallmark of malignancy, enables tumor cells to adapt to the harsh and dynamic tumor microenvironment (TME) by altering metabolic pathways. Hypoxia, prevalent in solid tumors, activates hypoxia inducible factor 1α (HIF-1α). HIF-1α drives metabolic reprogramming, enhancing glycolysis primarily through the Warburg effect to reduce oxygen dependence and facilitate tumor cell growth/proliferation. The above process is associated with accelerated tumor cell dedifferentiation and enhanced stemness, generating cancer stem cells (CSCs) which possesses the potential for self-renewal and differentiation that can differentiate into a wide range of subtypes of tumor cells and fuel tumor heterogeneity, metastasis, and recurrence, complicating therapy. This review examines the HIF-1α-glycolysis-dedifferentiation crosstalk mechanisms, expecting that indirect inhibition of HIF-1α by targeting metabolic enzymes, metabolites, or their signaling pathways will offer an effective therapeutic strategy to improve the cancer treatment outcomes.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"197 ","pages":"Pages 1-10"},"PeriodicalIF":3.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ferroptosis has been confirmed to be one of the key mechanisms of neuronal injury and dysfunction after spinal cord injury (SCI). Mechanical stresses such as deformation, compression, and stretching not only directly cause physical damage to spinal cord tissue at the moment of SCI, but also promote the development of ferroptosis through various pathways. However, the mechanism of ferroptosis after SCI remains unclear, which hinders the development of therapeutic methods.
Objective
This article aims to review the key mechanisms by which mechanical stress affects ferroptosis after SCI, including its impact on the structure and function of the endoplasmic reticulum (ER) and mitochondria, its role in triggering inflammatory responses, and its activation of mechanosensitive channels. Special emphasis is placed on the role of Piezo1 channels, which are key factors in cell mechanosensation and ion homeostasis regulation. The review explores how Piezo1 channels are upregulated by mechanical stress after SCI and participate in the ferroptosis process by mediating ion flow and other mechanisms.
Conclusions
Inhibiting Piezo1 channels may be a potential therapeutic strategy for SCI. This review summarizes the therapeutic potential of Piezo1 inhibitors by sorting out existing studies, hoping to provide a theoretical basis for effective therapeutic strategies targeting ferroptosis after SCI.
{"title":"The key role of Piezo1 channels in ferroptosis after spinal cord injury and the therapeutic potential of Piezo1 inhibitors","authors":"Qianxi Li, Chenyu Li, Xinyu Liu, Zixuan Guo, Xinxin Li, Xin Zhang","doi":"10.1016/j.pbiomolbio.2025.05.001","DOIUrl":"10.1016/j.pbiomolbio.2025.05.001","url":null,"abstract":"<div><h3>Background</h3><div>Ferroptosis has been confirmed to be one of the key mechanisms of neuronal injury and dysfunction after spinal cord injury (SCI). Mechanical stresses such as deformation, compression, and stretching not only directly cause physical damage to spinal cord tissue at the moment of SCI, but also promote the development of ferroptosis through various pathways. However, the mechanism of ferroptosis after SCI remains unclear, which hinders the development of therapeutic methods.</div></div><div><h3>Objective</h3><div>This article aims to review the key mechanisms by which mechanical stress affects ferroptosis after SCI, including its impact on the structure and function of the endoplasmic reticulum (ER) and mitochondria, its role in triggering inflammatory responses, and its activation of mechanosensitive channels. Special emphasis is placed on the role of Piezo1 channels, which are key factors in cell mechanosensation and ion homeostasis regulation. The review explores how Piezo1 channels are upregulated by mechanical stress after SCI and participate in the ferroptosis process by mediating ion flow and other mechanisms.</div></div><div><h3>Conclusions</h3><div>Inhibiting Piezo1 channels may be a potential therapeutic strategy for SCI. This review summarizes the therapeutic potential of Piezo1 inhibitors by sorting out existing studies, hoping to provide a theoretical basis for effective therapeutic strategies targeting ferroptosis after SCI.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"196 ","pages":"Pages 132-140"},"PeriodicalIF":3.2,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143924094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-16DOI: 10.1016/j.pbiomolbio.2025.04.003
Ashiq Ali , Urooj Azmat , Aisha Khatoon , Kaynaat Akbar , Bilal Murtaza , Ziyi Ji , Urooj Irshad , Zhongjing Su
Cancer continues to be a significant worldwide health concern, characterized by high rates of occurrence and death. Unfortunately, existing treatments frequently fall short of delivering satisfying therapeutic outcomes. Immunotherapy has ushered in a new era in the treatment of solid tumors, yet its effectiveness is still constrained and comes with unwanted side effects. The advancement of cutting-edge technology, propelled by gene analysis and manipulation at the molecular scale, shows potential for enhancing these therapies. The advent of genome editing technologies, including CRISPR-Cas9, can greatly augment the efficacy of cancer immunotherapy. This review explores the mechanism of CRISPR-Cas9-mediated genome editing and its wide range of tools. The study focuses on analyzing the effects of CRISPR-induced double-strand breaks (DSBs) on cancer immunotherapy, specifically by gene knockdown or knockin. In addition, the study emphasizes the utilization of CRISPR-Cas9-based genome-wide screening to identify targets, the potential of spatial CRISPR genomics, and the extensive applications and difficulties of CRISPR-Cas9 in fundamental research, translational medicine, and clinical environments.
{"title":"From gene editing to tumor eradication: The CRISPR revolution in cancer therapy","authors":"Ashiq Ali , Urooj Azmat , Aisha Khatoon , Kaynaat Akbar , Bilal Murtaza , Ziyi Ji , Urooj Irshad , Zhongjing Su","doi":"10.1016/j.pbiomolbio.2025.04.003","DOIUrl":"10.1016/j.pbiomolbio.2025.04.003","url":null,"abstract":"<div><div>Cancer continues to be a significant worldwide health concern, characterized by high rates of occurrence and death. Unfortunately, existing treatments frequently fall short of delivering satisfying therapeutic outcomes. Immunotherapy has ushered in a new era in the treatment of solid tumors, yet its effectiveness is still constrained and comes with unwanted side effects. The advancement of cutting-edge technology, propelled by gene analysis and manipulation at the molecular scale, shows potential for enhancing these therapies. The advent of genome editing technologies, including CRISPR-Cas9, can greatly augment the efficacy of cancer immunotherapy. This review explores the mechanism of CRISPR-Cas9-mediated genome editing and its wide range of tools. The study focuses on analyzing the effects of CRISPR-induced double-strand breaks (DSBs) on cancer immunotherapy, specifically by gene knockdown or knockin. In addition, the study emphasizes the utilization of CRISPR-Cas9-based genome-wide screening to identify targets, the potential of spatial CRISPR genomics, and the extensive applications and difficulties of CRISPR-Cas9 in fundamental research, translational medicine, and clinical environments.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"196 ","pages":"Pages 114-131"},"PeriodicalIF":3.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143854382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-10DOI: 10.1016/j.pbiomolbio.2025.04.002
Yeying Teng , Haiping Xue , Xiaoliang Deng , Yanqun Luo , Tao Wu
This article focuses on the phosphatidylethanolamine-binding protein (PEBP) family proteins, detailing PEBP1 and PEBP4 due to limited information on PEBP2 and PEBP3, in cellular signaling pathways and research in a spectrum of pathologies, including diverse cancers, metabolic disorders, immunological diseases and a subset of organ-specific diseases. It outlines the mechanisms through which PEBP1 and PEBP4 regulate essential signaling pathways that are critical for cellular processes such as proliferation, apoptosis, and metastasis. Recent advancements have shown further understanding of these proteins' roles in pathophysiology and their potential as future therapeutic targets. The findings suggest that the impact of PEBP1 and PEBP4 on the course of different diseases has underscored their potential for more in-depth medical research and novel clinically targeted therapies.
{"title":"The role of phosphatidylethanolamine-binding protein (PEBP) family in various diseases: Mechanisms and therapeutic potential","authors":"Yeying Teng , Haiping Xue , Xiaoliang Deng , Yanqun Luo , Tao Wu","doi":"10.1016/j.pbiomolbio.2025.04.002","DOIUrl":"10.1016/j.pbiomolbio.2025.04.002","url":null,"abstract":"<div><div>This article focuses on the phosphatidylethanolamine-binding protein (PEBP) family proteins, detailing PEBP1 and PEBP4 due to limited information on PEBP2 and PEBP3, in cellular signaling pathways and research in a spectrum of pathologies, including diverse cancers, metabolic disorders, immunological diseases and a subset of organ-specific diseases. It outlines the mechanisms through which PEBP1 and PEBP4 regulate essential signaling pathways that are critical for cellular processes such as proliferation, apoptosis, and metastasis. Recent advancements have shown further understanding of these proteins' roles in pathophysiology and their potential as future therapeutic targets. The findings suggest that the impact of PEBP1 and PEBP4 on the course of different diseases has underscored their potential for more in-depth medical research and novel clinically targeted therapies.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"196 ","pages":"Pages 102-113"},"PeriodicalIF":3.2,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-02DOI: 10.1016/j.pbiomolbio.2025.04.001
Jia Zhang , Runting Yin , Yongwang Xue , Rong Qin , Xuequan Wang , Shuming Wu , Jun Zhu , Yan-Shuang Li , Cai Zhang , Yuan Wei
Epithelial-mesenchymal transition (EMT) has been extensively studied for its roles in tumor metastasis, the generation and maintenance of cancer stem cells and treatment resistance. Epithelial mesenchymal plasticity allows cells to switch between various states within the epithelial-mesenchymal spectrum, resulting in a mixed epithelial/mesenchymal phenotypic profile. This plasticity underlies the acquisition of multiple malignant features during cancer progression and poses challenges for EMT in tumors. MicroRNAs (miRNAs) in the microenvironment affect numerous signaling processes through diverse mechanisms, influencing physiological activities. This paper reviews recent advances in EMT, the role of different hybrid states in tumor progression, and the important role of miRNAs in EMT. Furthermore, it explores the relationship between miRNA-based EMT therapies and their implications for clinical practice, discussing how ongoing developments may enhance therapeutic outcomes.
{"title":"Advances in the study of epithelial mesenchymal transition in cancer progression: Role of miRNAs","authors":"Jia Zhang , Runting Yin , Yongwang Xue , Rong Qin , Xuequan Wang , Shuming Wu , Jun Zhu , Yan-Shuang Li , Cai Zhang , Yuan Wei","doi":"10.1016/j.pbiomolbio.2025.04.001","DOIUrl":"10.1016/j.pbiomolbio.2025.04.001","url":null,"abstract":"<div><div>Epithelial-mesenchymal transition (EMT) has been extensively studied for its roles in tumor metastasis, the generation and maintenance of cancer stem cells and treatment resistance. Epithelial mesenchymal plasticity allows cells to switch between various states within the epithelial-mesenchymal spectrum, resulting in a mixed epithelial/mesenchymal phenotypic profile. This plasticity underlies the acquisition of multiple malignant features during cancer progression and poses challenges for EMT in tumors. MicroRNAs (miRNAs) in the microenvironment affect numerous signaling processes through diverse mechanisms, influencing physiological activities. This paper reviews recent advances in EMT, the role of different hybrid states in tumor progression, and the important role of miRNAs in EMT. Furthermore, it explores the relationship between miRNA-based EMT therapies and their implications for clinical practice, discussing how ongoing developments may enhance therapeutic outcomes.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"196 ","pages":"Pages 69-90"},"PeriodicalIF":3.2,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号