Biochimica et biophysica acta. Reviews on cancer最新文献

{"title":"Advancing cancer therapy: Mechanisms, efficacy, and limitations of calcium electroporation","authors":"Anna Szewczyk ,&nbsp;Dagmara Baczyńska ,&nbsp;Anna Choromańska ,&nbsp;Zofia Łapińska ,&nbsp;Agnieszka Chwiłkowska ,&nbsp;Jolanta Saczko ,&nbsp;Julita Kulbacka","doi":"10.1016/j.bbcan.2025.189319","DOIUrl":"10.1016/j.bbcan.2025.189319","url":null,"abstract":"<div><div>Calcium electroporation, an innovative technique, uses high-voltage pulses to introduce calcium ions into cells, leading to cell death and tumor growth inhibition. This review explores the potential of calcium electroporation as a promising therapeutic approach in cancer treatment. We provide an in-depth analysis of the underlying mechanisms by which calcium ions function within cells and how their introduction through electroporation can effectively induce cell death in cancer cells. Furthermore, we present a comprehensive overview of the current literature, covering both preclinical and clinical studies, to highlight the safety and efficacy of calcium electroporation in various cancer types, including melanoma, head and neck cancer, and breast cancer. We also discuss the distinct advantages of calcium electroporation over traditional cancer therapies, such as its specific targeting of cancer cells while sparing healthy cells. However, we also address the challenges and limitations associated with this technique, underscoring the need for further research. By providing a comprehensive examination of calcium electroporation, this review aims to contribute to understanding this emerging field and encourage further investigation into its potential as a novel cancer treatment strategy.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189319"},"PeriodicalIF":9.7,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143854905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological mechanisms and immunotherapy of brain metastases in non-small cell lung cancer","authors":"Sitong Jiang,&nbsp;Fengzhu Guo,&nbsp;Lin Li","doi":"10.1016/j.bbcan.2025.189320","DOIUrl":"10.1016/j.bbcan.2025.189320","url":null,"abstract":"<div><div>Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality worldwide, with Brain Metastases serving as a significant adverse prognostic factor. The blood-brain barrier poses a substantial challenge in the treatment of brain metastases, as it restricts the penetration of many anticancer agents. Novel immunotherapy, such as immune checkpoint inhibitors (ICIs) have emerged as promising treatment for NSCLC and its associated brain metastases. This review summarizes the biological mechanism underlying NSCLC brain metastases and provides an overview of the current landscape of immunotherapy, exploring the mechanism of action and clinical applications of these advanced treatments.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189320"},"PeriodicalIF":9.7,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143877334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Citrate oscillations during cell cycle are a targetable vulnerability in cancer cells","authors":"Philippe Icard ,&nbsp;Marco Alifano ,&nbsp;Luca Simula","doi":"10.1016/j.bbcan.2025.189313","DOIUrl":"10.1016/j.bbcan.2025.189313","url":null,"abstract":"<div><div>Cell cycle progression is timely interconnected with oscillations in cellular metabolism. Here, we first describe how these metabolic oscillations allow cycling cells to meet the bioenergetic needs specifically for each phase of the cell cycle. In parallel, we highlight how the cytosolic level of citrate is dynamically regulated during these different phases, being low in G1 phase, increasing in S phase, peaking in G2/M, and decreasing in mitosis. Of note, in cancer cells, a dysregulation of such citrate oscillation can support cell cycle progression by promoting a deregulated Warburg effect (aerobic glycolysis), activating oncogenic signaling pathways (such as PI3K/AKT), and promoting acetyl-CoA production via alternative routes, such as overconsumption of acetate. Then, we review how administration of sodium citrate (at high doses) arrests the cell cycle in G0/G1 or G2/M, inhibits glycolysis and PI3K/AKT, induces apoptosis, and significantly reduces tumor growth in various in vivo models. Last, we reason on the possibility to implement citrate administration to reinforce the effectiveness of cell cycle inhibitors to better cure cancer.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189313"},"PeriodicalIF":9.7,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles as the common denominator among the 7 Rs of radiobiology: From the cellular level to clinical practice","authors":"Júlia Oliveira Dias ,&nbsp;Igor Sampaio Fagundes ,&nbsp;Mariana de Cássia Bisio ,&nbsp;Victoria da Silva Barboza ,&nbsp;Alexandre Arthur Jacinto ,&nbsp;Wanessa Fernanda Altei","doi":"10.1016/j.bbcan.2025.189315","DOIUrl":"10.1016/j.bbcan.2025.189315","url":null,"abstract":"<div><div>Extracellular vesicles (EVs) are lipid-bound particles released by tumor cells and widely explored in cancer development, progression, and treatment response, being considered as valuable components to be explored as biomarkers or cellular targets to modulate the effect of therapies. The mechanisms underlying the production and profile of EVs during radiotherapy (RT) require addressing radiobiological aspects to determine cellular responses to specific radiation doses and fractionation. In this review, we explore the role of EVs in the 7 Rs of radiobiology, known as the molecular basis of a biological tissue response to radiation, supporting EVs as a shared player in all the seven processes. We also highlight the relevance of EVs in the context of liquid biopsy and resistance to immunotherapy, aiming to establish the connection and utility of EVs as tools in contemporary and precision radiotherapy.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189315"},"PeriodicalIF":9.7,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143825525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PAQR4: From spatial regulation of cell signaling to physiological homeostasis and diseases","authors":"Zi-Yan Jin ,&nbsp;Zhi-Qiang Ling","doi":"10.1016/j.bbcan.2025.189314","DOIUrl":"10.1016/j.bbcan.2025.189314","url":null,"abstract":"<div><div>Progestin and adipoQ receptor family member 4 (PAQR4) gene is a recently discovered seven-transmembrane protein-coding gene that belongs to the PAQR family. An increasing amount of evidence suggests that PAQR4 is upregulated in multiple tumors and participates in tumor progression and chemotherapy resistance via different signaling pathways; PAQR4 regulates cellular ceramide homeostasis by influencing sphingolipid metabolism and glycerol metabolism, and plays a significant role in adipose tissue remodeling. Meanwhile, it is known that the differential expression of PAQR4 is associated with the occurrence of various diseases and is a potential biomarker and therapeutic target. This article conducts a systematic review of the subcellular localization of PAQR4, its topological structure characteristics, and its functions in cancer occurrence, metabolic diseases, and fertility, and provides clues for the future research and translational application of PAQR4.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189314"},"PeriodicalIF":9.7,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tertiary lymphoid structures achieve ‘cold’ to ‘hot’ transition by remodeling the cold tumor microenvironment","authors":"Mengke Cui ,&nbsp;Mengfan Zhou ,&nbsp;Lu Zhou ,&nbsp;Gan Zhou ,&nbsp;Yingzi Liu","doi":"10.1016/j.bbcan.2025.189312","DOIUrl":"10.1016/j.bbcan.2025.189312","url":null,"abstract":"<div><div>Immune checkpoint blockade (ICB) therapies have demonstrated significant clinical efficacy in immune-infiltrated tumors such as melanoma and non-small cell lung cancer. However, “cold tumors”—including ovarian cancer, pancreatic cancer, and gliomas—exhibit insufficient immune infiltration, leading to poor therapeutic responses to ICBs and limited improvement in patient prognosis. Recent studies have shown that tumor-associated tertiary lymphoid structures (TLSs) can induce strong local immune responses within the tumor microenvironment (TME), serving as important biological markers for predicting ICB therapy efficacy. Notably, preclinical and clinical studies on cold tumors have confirmed that TLSs can potently enhance ICB efficacy through TME remodeling—a breakthrough that has attracted considerable attention. Here, we systematically examine the immunological profile of cold tumors and decipher the mechanistic basis for their impaired immune cell infiltration. We further delineate the distinctive features of tumor-associated TLSs in generating antitumor immunity and establish criteria for their identification. Significantly, we emphasize the unique capability of TLSs to reprogram the immunosuppressive tumor microenvironment characteristic of cold tumors. Based on these insights, we evaluate clinical evidence supporting TLS-mediated enhancement of ICB efficacy and discuss emerging strategies for exogenous TLSs induction.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189312"},"PeriodicalIF":9.7,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myeloid cells in the microenvironment of brain metastases","authors":"Nian Chen ,&nbsp;Tao Zhang ,&nbsp;Xianyan Yang ,&nbsp;Di Wang ,&nbsp;Shicang Yu","doi":"10.1016/j.bbcan.2025.189311","DOIUrl":"10.1016/j.bbcan.2025.189311","url":null,"abstract":"<div><div>Brain metastasis (BrM) from peripheral solid tumors has a high mortality rate and remains a daunting clinical challenge. In addition to the targeting of tumor cells, studies have focused on the regulation of the tumor microenvironment (TME) for BrM treatment. Here, through a review of recent studies, we revealed that myeloid infiltration is a common feature of the TME in BrMs from different primary sites even though the brain is regarded as an immune-privileged site and is always in an immunosuppressive state. Tumor-educated bone marrow progenitors, especially mesenchymal stem cells (MSCs), may impact the brain tropism and and phenotypic switching of myeloid cells. Additionally, chronic inflammation may be key factors regulating the immunosuppressive TME and myeloid cell reprogramming. Here, the role of myeloid cells in the formation of the TME and strategies for targeting these cells before and after BrM are reviewed, emphasizing the potential for the use of myeloid cells in BrM treatment. However, the direct relationship between the neuronal system and myeloid cell filtration is still unclear and worthy of further study.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189311"},"PeriodicalIF":9.7,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sorafenib resistance and therapeutic strategies in hepatocellular carcinoma","authors":"Weijing Zhang ,&nbsp;Xuechuan Hong ,&nbsp;Yuling Xiao ,&nbsp;Hongbo Wang ,&nbsp;Xiaodong Zeng","doi":"10.1016/j.bbcan.2025.189310","DOIUrl":"10.1016/j.bbcan.2025.189310","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) remains one of the most prevalent and lethal cancers globally. While surgical resection and liver transplantation offer potential cures for early-stage HCC, the majority of patients are diagnosed at advanced stages where such interventions are not viable. Sorafenib, a multi-target kinase inhibitor, has been a cornerstone in the treatment of advanced HCC since its approval in 2007. Despite its significant clinical impact, less than half of the treated patients derive long-term benefits due to the emergence of resistance and associated side effects. This review focuses on the role of sorafenib, an FDA-approved multi-target kinase inhibitor, in treating advanced HCC, discusses the mechanisms underlying its therapeutic effects and associated resistance, and explores additional therapeutic strategies being investigated to improve patient outcomes.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189310"},"PeriodicalIF":9.7,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The crosstalk within tumor microenvironment and exosomes in pancreatic cancer","authors":"Michael Ochieng' Otieno ,&nbsp;Tomasz Powrózek ,&nbsp;Jesus Garcia-Foncillas ,&nbsp;Javier Martinez-Useros","doi":"10.1016/j.bbcan.2025.189308","DOIUrl":"10.1016/j.bbcan.2025.189308","url":null,"abstract":"<div><div>Pancreatic cancer is one of the most malignant tumors with a grim prognosis. Patients develop chemoresistance that drastically decreases their survival. The chemoresistance is mainly attributed to deficient vascularization of the tumor, intratumoral heterogeneity and pathophysiological barrier due to the highly desmoplastic tumor microenvironment. The interactions of cells that constitute the tumor microenvironment change its architecture into a cancer-permissive environment and stimulate cancer development, metastasis and treatment response. The cell-cell communication in the tumor microenvironment is often mediated by exosomes that harbour a diverse repertoire of molecular cargo, such as proteins, lipids, and nucleic acid, including messenger RNAs, non-coding RNAs and DNA. Therefore, exosomes can serve as potential targets as biomarkers and improve the clinical management of pancreatic cancer to overcome chemoresistance. This review critically elucidates the role of exosomes in cell-cell communication within the tumor microenvironment and how these interactions can orchestrate chemoresistance.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189308"},"PeriodicalIF":9.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The epipliancy journey: Tumor initiation at the mercy of identity crisis and epigenetic drift","authors":"Rahma Benhassoun ,&nbsp;Anne-Pierre Morel ,&nbsp;Victoria Jacquot ,&nbsp;Alain Puisieux ,&nbsp;Maria Ouzounova","doi":"10.1016/j.bbcan.2025.189307","DOIUrl":"10.1016/j.bbcan.2025.189307","url":null,"abstract":"<div><div>Cellular pliancy refers to the unique disposition of different stages of cellular differentiation to transform when exposed to specific oncogenic insults. This concept highlights a strong interconnection between cellular identity and tumorigenesis, and implies overcoming of epigenetic barriers defining cellular states. Emerging evidence suggests that the cell-type-specific response to intrinsic and extrinsic stresses is modulated by accessibility to certain areas of the genome. Understanding the interplay between epigenetic mechanisms, cellular differentiation, and oncogenic insults is crucial for deciphering the complex nature of tumorigenesis and developing targeted therapies. Hence, cellular pliancy relies on a dynamic cooperation between the cellular identity and the cellular context through epigenetic control, including the reactivation of cellular mechanisms, such as epithelial-to-mesenchymal transition (EMT). Such mechanisms and pathways confer plasticity to the cell allowing it to adapt to a hostile environment in a context of tumor initiation, thus changing its cellular identity.</div><div>Indeed, growing evidence suggests that cancer is a disease of cell identity crisis, whereby differentiated cells lose their defined identity and gain progenitor characteristics. The loss of cell fate commitment is a central feature of tumorigenesis and appears to be a prerequisite for neoplastic transformation. In this context, EMT-inducing transcription factors (EMT-TFs) cooperate with mitogenic oncoproteins to foster malignant transformation. The aberrant activation of EMT-TFs plays an active role in tumor initiation by alleviating key oncosuppressive mechanisms and by endowing cancer cells with stem cell-like properties, including the ability to self-renew, thus changing the course of tumorigenesis. This highly dynamic phenotypic change occurs concomitantly to major epigenome reorganization, a key component of cell differentiation and cancer cell plasticity regulation.</div><div>The concept of pliancy was initially proposed to address a fundamental question in cancer biology: why are some cells more likely to become cancerous in response to specific oncogenic events at particular developmental stages? We propose the concept of epipliancy, whereby a difference in epigenetic configuration leads to malignant transformation following an oncogenic insult. Here, we present recent studies furthering our understanding of how the epigenetic landscape may impact the modulation of cellular pliancy during early stages of cancer initiation.</div></div>","PeriodicalId":8782,"journal":{"name":"Biochimica et biophysica acta. Reviews on cancer","volume":"1880 3","pages":"Article 189307"},"PeriodicalIF":9.7,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}