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}
Pub Date : 2025-03-28DOI: 10.1016/j.pbiomolbio.2025.03.001
Alessandro Maria Morelli , Ann Saada , Felix Scholkmann
There are several physiological reasons why biological organisms sleep. One key one concerns brain metabolism. In our article we discuss the role of metabolism in myelin, based on the recent discovery that myelin contains mitochondrial components that enable the production of adenosine triphosphate (ATP) via oxidative phosphorylation (OXPHOS). These mitochondrial components in myelin probably originate from vesiculation of the mitochondrial membranes in form from mitochondrial derived vesicles (MDVs). We hypothesize that myelin acts as a proton capacitor, accumulating energy in the form of protons during sleep and converting it to ATP via OXPHOS during wakefulness. Empirical evidence supporting our hypothesis is discussed, including data on myelin metabolic activity, MDVs, and allometric scaling between white matter volume and sleep duration in mammals.
{"title":"Myelin: A possible proton capacitor for energy storage during sleep and energy supply during wakefulness","authors":"Alessandro Maria Morelli , Ann Saada , Felix Scholkmann","doi":"10.1016/j.pbiomolbio.2025.03.001","DOIUrl":"10.1016/j.pbiomolbio.2025.03.001","url":null,"abstract":"<div><div>There are several physiological reasons why biological organisms sleep. One key one concerns brain metabolism. In our article we discuss the role of metabolism in myelin, based on the recent discovery that myelin contains mitochondrial components that enable the production of adenosine triphosphate (ATP) via oxidative phosphorylation (OXPHOS). These mitochondrial components in myelin probably originate from vesiculation of the mitochondrial membranes in form from mitochondrial derived vesicles (MDVs). We hypothesize that myelin acts as a proton capacitor, accumulating energy in the form of protons during sleep and converting it to ATP via OXPHOS during wakefulness. Empirical evidence supporting our hypothesis is discussed, including data on myelin metabolic activity, MDVs, and allometric scaling between white matter volume and sleep duration in mammals.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"196 ","pages":"Pages 91-101"},"PeriodicalIF":3.2,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744519","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 : 2025-02-27DOI: 10.1016/j.pbiomolbio.2025.02.004
Polina Vertegel , Pavel Milkin , Anton Murashko , Mikhail Parker , Kristina Peranidze , Natalia Emashova , Sergiy Minko , Vladimir Reukov
Culturing living cells outside the body is a complex process involving various techniques. Despite advances, harvesting cells remains challenging, especially in light of new emerging and scaled-up cell culture technologies. Enzymatic adherent cell harvesting is the most used and robust technology but can harm cells. Non-enzymatic detachment methods offer advantages but also present challenges. Thermo-responsive polymers require precise control of the molecular characteristics and thickness of the thermoresponsive films, which makes this method less robust and more expensive. This review highlights the importance of controlling harvested cell quality and its relationship to cell binding and detachment mechanisms. Many alternative methods have not been extensively analyzed, and their impact on cell quality beyond standard viability assays is not yet known. Developing robust cell harvesting methods for bioreactor microcarriers is a rapidly growing challenge as the cell manufacturing industry expands. Microcarriers with stimuli-responsive coatings face challenges similar to those observed for laboratory-scale cell dishes and bring an additional aspect of the need for microbead recycling consideration. All that together underlines the importance of the research in biomaterials and biotechnology for cell manufacturing.
{"title":"Cell detachment: A review of techniques, challenges, and opportunities for advancing biomedical research and applications","authors":"Polina Vertegel , Pavel Milkin , Anton Murashko , Mikhail Parker , Kristina Peranidze , Natalia Emashova , Sergiy Minko , Vladimir Reukov","doi":"10.1016/j.pbiomolbio.2025.02.004","DOIUrl":"10.1016/j.pbiomolbio.2025.02.004","url":null,"abstract":"<div><div>Culturing living cells outside the body is a complex process involving various techniques. Despite advances, harvesting cells remains challenging, especially in light of new emerging and scaled-up cell culture technologies. Enzymatic adherent cell harvesting is the most used and robust technology but can harm cells. Non-enzymatic detachment methods offer advantages but also present challenges. Thermo-responsive polymers require precise control of the molecular characteristics and thickness of the thermoresponsive films, which makes this method less robust and more expensive. This review highlights the importance of controlling harvested cell quality and its relationship to cell binding and detachment mechanisms. Many alternative methods have not been extensively analyzed, and their impact on cell quality beyond standard viability assays is not yet known. Developing robust cell harvesting methods for bioreactor microcarriers is a rapidly growing challenge as the cell manufacturing industry expands. Microcarriers with stimuli-responsive coatings face challenges similar to those observed for laboratory-scale cell dishes and bring an additional aspect of the need for microbead recycling consideration. All that together underlines the importance of the research in biomaterials and biotechnology for cell manufacturing.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"196 ","pages":"Pages 50-68"},"PeriodicalIF":3.2,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537855","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 : 2025-02-21DOI: 10.1016/j.pbiomolbio.2025.02.003
Tanvi Gupta , Mohd Murtaza
Pancreatic cancer is one of the most deadly with poor prognosis and overall survival rate due to the dense stroma in the tumors which often is challenging for the delivery of drug to penetrate deep inside the tumor bed and usually results in the progression of cancer. The conventional treatment such as chemotherapy, radiotherapy or surgery shows a minimal benefit in the survival due to the drug resistance, poor penetration, less radiosensitivity or recurrence of tumor. There is an urgent demand to develop molecular-level targeted therapies to achieve therapeutic efficacy in the pancreatic ductal adenocarcinoma (PDAC) patients. The precision oncology focuses on the unique attributes of the patient such as epigenome, proteome, genome, microbiome, lifestyle and diet habits which contributes to promote oncogenesis. The targeted therapy helps to target the mutated proteins responsible for controlling growth, division and metastasis of tumor in the cancer cells. It is very important to consider all the attributes of the patient to provide the suitable personalized treatment to avoid any severe side effects. In this review, we have laid emphasis on the precision medicine; the utmost priority is to improve the survival of cancer patients by targeting molecular mutations through transmembrane proteins, inhibitors, signaling pathways, immunotherapy, gene therapy or the use of nanocarriers for the delivery at the tumor site. It will become beneficial therapeutic window to be considered for the advanced stage pancreatic cancer patients to prolong their survival rate.
{"title":"Advancing targeted therapies in pancreatic cancer: Leveraging molecular abberrations for therapeutic success","authors":"Tanvi Gupta , Mohd Murtaza","doi":"10.1016/j.pbiomolbio.2025.02.003","DOIUrl":"10.1016/j.pbiomolbio.2025.02.003","url":null,"abstract":"<div><div>Pancreatic cancer is one of the most deadly with poor prognosis and overall survival rate due to the dense stroma in the tumors which often is challenging for the delivery of drug to penetrate deep inside the tumor bed and usually results in the progression of cancer. The conventional treatment such as chemotherapy, radiotherapy or surgery shows a minimal benefit in the survival due to the drug resistance, poor penetration, less radiosensitivity or recurrence of tumor. There is an urgent demand to develop molecular-level targeted therapies to achieve therapeutic efficacy in the pancreatic ductal adenocarcinoma (PDAC) patients. The precision oncology focuses on the unique attributes of the patient such as epigenome, proteome, genome, microbiome, lifestyle and diet habits which contributes to promote oncogenesis. The targeted therapy helps to target the mutated proteins responsible for controlling growth, division and metastasis of tumor in the cancer cells. It is very important to consider all the attributes of the patient to provide the suitable personalized treatment to avoid any severe side effects. In this review, we have laid emphasis on the precision medicine; the utmost priority is to improve the survival of cancer patients by targeting molecular mutations through transmembrane proteins, inhibitors, signaling pathways, immunotherapy, gene therapy or the use of nanocarriers for the delivery at the tumor site. It will become beneficial therapeutic window to be considered for the advanced stage pancreatic cancer patients to prolong their survival rate.</div></div>","PeriodicalId":54554,"journal":{"name":"Progress in Biophysics & Molecular Biology","volume":"196 ","pages":"Pages 19-32"},"PeriodicalIF":3.2,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143484597","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}