Experimental cell research最新文献

{"title":"Cancer as a failed response to renegade mitochondria","authors":"John Hartung","doi":"10.1016/j.yexcr.2025.114721","DOIUrl":"10.1016/j.yexcr.2025.114721","url":null,"abstract":"<div><div>In 1948, before the word ‘mitochondrion’ gained common parlance in the lexicon of cell biologists, Cyril Darlington published <em>The Plasmagene Theory of the Origin of Cancer</em> without referring to mitochondria <em>per se</em>. Reconsideration of Darlington's theory is warranted today because discoveries about the extraordinary capacities of mitochondria – the organelles that house Darlington's “plasmagenes” – have grown exponentially.</div><div>If Darlington was right, if intracellular competition between mutant and wild-type mitochondria is the first cause of cancer, it may be the case that a general cure for cancer will include injection of: (A) nanoparticles carrying wild-type mitochondrial genes, and (B) copious amounts of wild-type mitochondria.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 2","pages":"Article 114721"},"PeriodicalIF":3.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893190","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}

{"title":"Cryptotanshinone instigates ferroptosis to inhibit the development of tamoxifen-resistant breast cancer via the AMPK induced BECN1-SLC7A11 complex axis","authors":"Mengning Zhang ,&nbsp;Hang Chen ,&nbsp;Lujia Zhang ,&nbsp;Aini Yuan ,&nbsp;Jing Liu ,&nbsp;Qi Wang ,&nbsp;Tiantian Lei ,&nbsp;Hong Zhao","doi":"10.1016/j.yexcr.2025.114726","DOIUrl":"10.1016/j.yexcr.2025.114726","url":null,"abstract":"<div><div>The resistance of oestrogen receptor-positive (ER+) breast cancer to tamoxifen (TAM) therapy represents a significant challenge in the clinical management of ER + breast cancer. It has been demonstrated that tamoxifen-resistant breast cancer is sensitive to ferroptosis. Consequently, the targeted intervention of Solute Carrier Family 7 Member 11 (SLC7A11) to promote ferroptosis represents a promising means of treating this form of cancer. Cryptotanshinone (CTS), a fat-soluble diterpene derivative extracted from Salvia miltiorrhiza, has been demonstrated to possess favorable anti-breast cancer activity. However, it remains unclear whether CTS is effective against tamoxifen-resistant breast cancer. The objective of this study was to ascertain whether CTS-induced ferroptosis could be employed to inhibit tamoxifen-resistant breast cancer, and to elucidate the potential mechanism of action. CTS was observed to inhibit the proliferation of TAM-resistant MCF-7 cells, and this effect could be synergistically amplified by co-treatment with TAM. Furthermore, CTS was also demonstrated to increase the sensitivity of TAM-resistant MCF-7 cells to TAM. Additionally, CTS has been observed to promote ferroptosis in TAM-resistant MCF-7 cells, resulting in elevated levels of the associated indices 4 Hydroxynonenal (4HNE), Lipid Reactive oxygen species (ROS), ROS and Fe²⁺, while concurrently reducing the levels of SLC7A11 and Glutathione peroxidase 4 (GPX4). Further studies demonstrated that CTS promoted TAM-resistant MCF-7 cell ferroptosis based on the formation of the BECN1-SLC7A11 complex, which resulted in a decrease in SLC7A11. Validation experiments demonstrated that CTS-induced BECN1-SLC7A11 complex formation is dependent on AMPK activation. Xenotumour transplantation experiments revealed that CTS combined with TAM inhibits TAM-resistant breast cancer and promotes ferroptosis through the AMPK/BECN1/SLC7A11 axis. In conclusion, CTS retarded the growth of TAM-resistant breast cancer tumours by activating AMPK to promote the formation of the BECN1-SLC7A11 complex and inhibiting the expression of SLC7A11, thereby inducing ferroptosis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 2","pages":"Article 114726"},"PeriodicalIF":3.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144912356","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}

{"title":"FOXC1 and FOXC2 in Osteogenesis: Emerging roles and therapeutic potential in bone regeneration and remodeling","authors":"Ali Molaei ,&nbsp;Emad Molaei ,&nbsp;A. Wallace Hayes ,&nbsp;Gholamreza Karimi","doi":"10.1016/j.yexcr.2025.114712","DOIUrl":"10.1016/j.yexcr.2025.114712","url":null,"abstract":"<div><div>Bone is a remarkable dynamic tissue, continually undergoing intricate processes of development, repair, and lifelong remodeling, all vital for maintaining skeletal integrity, facilitating injury recovery, and preserving overall health. Mesenchymal stem cells (MSCs) are central to these processes, characterized by their self-renewal capacity, multipotent differentiation (including osteoblasts), and crucial roles in secreting growth factors and remodeling the extracellular matrix.</div><div>The highly conserved transcription factors FOXC1 and FOXC2 are crucial for correct skeletal development, profoundly influencing both intramembranous and endochondral ossification. Beyond these established developmental functions, recent evidence illuminates their critical emerging roles in actively regulating MSC osteogenic commitment and promoting osteoblastic differentiation, particularly in early cellular stages. FOXC1, for instance, orchestrates the expression of key osteogenic and chondrogenic transcription factors such as SOX9 (vital for endochondral ossification) and MSX2 (paramount in intramembranous bone formation). FOXC2, in turn, significantly contributes to osteoblast maturation through robust activation of the WNT/β-catenin signaling pathway. Furthermore, compelling experimental studies now directly implicate FOXC1 and FOXC2 in adult bone repair, the maintenance of bone mineral density (BMD), and the modulation of joint health. This bridges their developmental significance to substantial therapeutic potential in adult skeletal pathologies.</div><div>This review comprehensively synthesizes current understanding of the developmental and emerging adult roles of FOXC1 and FOXC2 in bone biology, with a focused exploration of their underlying molecular and cellular mechanisms in osteogenesis. We also critically discuss their promising therapeutic potential in prevalent skeletal conditions such as fractures, osteoporosis, and osteoarthritis, illustrating how insights from embryonic bone formation can directly inform novel strategies for enhancing adult bone regeneration and remodeling.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 2","pages":"Article 114712"},"PeriodicalIF":3.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144904176","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}

{"title":"Tumor suppressor OSR1 is modified by SUMO1 and regulates the Wnt/β-catenin signaling pathway in HCC.","authors":"Xinju Lin, Yuming Liu, Zisen Lai, Xiaopei Wang, Yongliang Cui, Shangeng Weng","doi":"10.1016/j.yexcr.2025.114693","DOIUrl":"10.1016/j.yexcr.2025.114693","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the deadliest cancers in the world. Exploring the underlying molecular mechanisms of HCC, such as those involving small ubiquitin-related modifier (SUMO) and its targets, is worthwhile. A total of 12 HCC tissue samples were collected for immunohistochemistry. The interaction between SUMO1 and OSR1 was confirmed by co-IP and immunofluorescence (IF). The expression (qPCR and Western blot), cytological function (CCK-8, clone formation and transwell assays) of OSR1 was further investigated in HepG2 cells. The anti-tumor function of OSR1 was also verified in the nude mouse xenograft model. Western blot analysis revealed the underlying downstream signaling pathway of SUMO1-modified OSR1 in HCC. Up-regulated co-expression of SUMO1-OSR1 was observed in the HepG2 cells. Through the cytological experiments and a nude mouse xenograft model, we found that OSR1 is a tumor suppressor gene that inhibits the proliferation and invasion of the HepG2 cells in vitro. Intriguingly, SUMO1-OE antagonized OSR1-mediated β-catenin regulation: in nuclei, SUMO1-OE enhanced β-catenin expression, counteracting OSR1-OE-induced suppression, whereas in the cytoplasm, SUMO1-OE inhibited β-catenin accumulation and attenuated OSR1-OE-driven promotion. Hypoxia reversed these effects, suggesting an oxygen-sensitive interplay between SUMO1 and OSR1. In conclusion, OSR1 is a tumor suppressor in HCC via attenuation of the Wnt/β-catenin pathway. SUMO1 modifies OSR1, suppressing the Wnt/β-catenin signaling pathway and promoting the occurrence and development of HCC; this effect of which could be enhanced by hypoxia.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114693"},"PeriodicalIF":3.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759585","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}

{"title":"Single cell RNA sequencing reveals shifts in cell maturity and function of endogenous and infiltrating cell types in response to acute intervertebral disc injury.","authors":"Sade W Clayton, Aimy Sebastian, Stephen P Wilson, Nicholas R Hum, Remy E Walk, Garrett W D Easson, Rachana Vaidya, Kaitlyn S Broz, Gabriela G Loots, Simon Y Tang","doi":"10.1016/j.yexcr.2025.114691","DOIUrl":"10.1016/j.yexcr.2025.114691","url":null,"abstract":"<p><p>Intervertebral disc (IVD) degeneration contributes to disabling back pain. Degeneration can be initiated by injury and progressively leads to an irreversible loss of cells and function. IVD function restoration through cell replacement therapies have had limited success due to knowledge gaps in the critical cell populations important for repair. Here, we used single cell RNA sequencing to identify the transcriptional changes of IVD resident and infiltrating cell populations from Control and Injured coccygeal IVDs extracted from 12-week-old female C57BL/6J mice 7 days post injury. Clustering, gene ontology, and pseudotime trajectory analyses determined transcriptomic divergences with injury, flow cytometry identified they types of infiltrating immune cells, and immunofluorescence was utilized to define mesenchymal stem cell (MSC) localization. We identified 11 distinct clusters that included IVD, immune, vascular cells, and MSCs. Differential gene expression analysis determined that Outer Annulus Fibrosus, Neutrophils, Saa2-High MSCs, Macrophages, and Krt18⁺ Nucleus Pulposus (NP) cells were the major drivers of transcriptomic differences between Control and Injured cells. Gene ontology revealed that the most upregulated biological pathways were angiogenesis and T cell-related while wound healing and ECM regulation were downregulated. Pseudotime trajectory analyses revealed that IVD injury directed cells towards increased differentiation in all clusters, except for Krt18⁺ NP cells which remained in a less mature cell state. Saa2-High and Grem1-High MSCs populations shifted towards more differentiated IVD cells profiles with injury and localized distinctly within the IVD. This study revealed novel MSC populations with the potential to be leveraged for future IVD repair studies.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114691"},"PeriodicalIF":3.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764800","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}

{"title":"Upregulation of Linc00960 promotes colorectal cancer cell proliferation by regulating hsa-miR-107/CDK6 axis","authors":"Chunlin Ke ,&nbsp;Peirong Wang ,&nbsp;Biao Chen ,&nbsp;Xianhui Cheng ,&nbsp;Xinyi Zhang ,&nbsp;Rongmu Xia ,&nbsp;Feng Dong ,&nbsp;Jiancheng Li","doi":"10.1016/j.yexcr.2025.114697","DOIUrl":"10.1016/j.yexcr.2025.114697","url":null,"abstract":"<div><div>Colorectal cancer (CRC), the most common gastrointestinal malignancy, has incompletely understood underlying developmental mechanisms. LincRNA, a subclass of long non-coding RNAs (LncRNAs), is implicated in the pathogenesis of multiple cancers, including CRC. In this study, qPCR analysis revealed that Linc00960 expression was significantly upregulated in CRC tissues compared to adjacent non-tumor tissues and correlated with poor patient prognosis. Functional assays (including cell proliferation, colony formation, flow cytometry, Transwell assay and xenograft experiments) demonstrated that high Linc00960 expression enhanced CRC cell proliferation, whereas Linc00960 knockdown markedly suppressed cell proliferation, migration and invasion. To investigate the mechanism, dual-luciferase reporter assays were performed; there revealed that Linc00960 directly bound to hsa-miR-107 (miR-107) and negatively regulated its expression, thereby upregulating CDK6 expression and promoting CRC cell proliferation. In conclusion, our findings indicated that the Linc00960/miR-107/CDK6 axis served as a crucial signaling pathway in CRC progression, providing novel potential targets and biomarkers for CRC diagnosis and therapy.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 1","pages":"Article 114697"},"PeriodicalIF":3.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144803898","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}

{"title":"Reduction in vinculin levels with Rb1 loss is responsible for altered differentiation in preosteoblasts","authors":"Elisha Pendleton,&nbsp;Keren Abdallah,&nbsp;Nalini Chandar","doi":"10.1016/j.yexcr.2025.114690","DOIUrl":"10.1016/j.yexcr.2025.114690","url":null,"abstract":"<div><div>We have shown previously that loss of Rb1 in osteoblasts results in changes to gap junctional intercellular communication and a decrease in membrane proteins such as connexin 43 and cadherin 11. These cells also start expressing adipocyte specific transcription factors and marker genes while continuing to express osteoblast specific differentiated features. The mechanistic reason for this shift in differentiation behavior is not known. Recent studies have suggested a role for vinculin, a protein component of focal adhesions, in the transduction of signals to YAP-TAZ transcription factors to suppress adipocyte differentiation and allow osteoblast differentiation. We found loss of Rb1 expression in osteoblasts dramatically reduced vinculin quantity, with less distribution within focal adhesions when tested by immunofluorescence. Vinculin levels steadily increased during in vitro osteoblast differentiation and were about 6-8-fold higher in differentiated osteoblasts. Rb1 deficient cells showed an increase albeit at reduced levels (2-4-fold) during differentiation. A corresponding increase in YAP-TAZ activity and expression were seen in control osteoblasts and a stunted but similar response was present in Rb1 deficient osteoblasts. The fact that Rb1 deficient osteoblasts respond by increasing vinculin levels suggests that they can maintain the expected functional changes at a reduced level. To demonstrate that the concentration of vinculin was the determining factor, we either over expressed or knocked down vinculin which resulted in appropriately altering YAP/TAZ activity. Increased vinculin expression enhanced osteogenic while inhibiting adipocytic gene expression. During osteoblast differentiation, TAZ can be clearly visualized in the nucleus in osteoblasts’ whereas with Rb1 deficiency the distribution was diffuse within the cells. The reduction in vinculin expression, combined with a feeble response in YAP-TAZ signaling activity, may explain the lack of complete inhibition of adipocyte specific gene expression and a generation of a mixed phenotype seen with loss of Rb1 function. As the adipocyte master transcription factor PPAR-gamma levels are increased by Rb1 loss, we knockdown PPAR-gamma which resulted in an increase to vinculin expression, showing that the PPAR-gamma induced activation of adipocyte differentiation pathway is responsible for reducing vinculin expression in RbKD cells.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 1","pages":"Article 114690"},"PeriodicalIF":3.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144780640","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}

{"title":"Circulating extrachromosomal circular DNA in epithelial ovarian cancer reflects chemotherapeutic response and recurrence","authors":"Jing Wang ,&nbsp;Zhicheng Xu ,&nbsp;Yan Zhong ,&nbsp;Jiaxuan Yang ,&nbsp;Zongle Yang ,&nbsp;Wei Ye ,&nbsp;Qiang Wu ,&nbsp;Youwen Du ,&nbsp;Jianghao Xing ,&nbsp;Mafei Xu","doi":"10.1016/j.yexcr.2025.114695","DOIUrl":"10.1016/j.yexcr.2025.114695","url":null,"abstract":"<div><div>Cell-free extrachromosomal circular DNA (eccDNA) in the plasma provides an advantage for monitoring epithelial ovarian cancer (EOC) progression. We isolated eccDNA from plasma samples of 30 EOC patients before treatment (T0 time point) and 4 healthy individuals. We followed 16 EOC patients, collecting paired eccDNA samples between the 3rd and 4th course of chemotherapy (T1) and 6 months after the last course of chemotherapy (F). The patients were divided into three groups, including complete remission (CR) group, partial remission group (PR), and relapse group (RC). We compared the normalized eccDNA count per million mapped reads (EPM) among all the groups and assessed the distribution of eccDNA on each chromosome. Then, the eccDNA within the top 5 % coverage regions of each chromosome were annotated, and the top genes were analyzed for prognosis. We found that EOC patients exhibited significantly higher levels of eccDNA, with higher coverage in coding exon regions. Notably, circulating eccDNA was generally increased in the CR group, while decreased in the PR and RC group during treatment. Our results showed that the fold change of EPMs between the T1 and T0 distinguished PR and RC patients from CR patients, with area under the curve (AUC) of 0.71. Additionally, we identified two genes, <em>SCARB1</em> and <em>PDE10A</em>, whose EPMs were able to predict prognosis in EOC patients, with AUCs of 0.86 and 0.83, respectively. Thus, our study offers valuable preliminary insights into a novel approach for predicting chemotherapy sensitivity in EOC patients, based on the trends of circulating eccDNA.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 1","pages":"Article 114695"},"PeriodicalIF":3.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144803897","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}

{"title":"The RNA-binding protein HuR regulates microRNA biogenesis via increased drosha expression","authors":"Lin Liu ,&nbsp;Linxiao Wang ,&nbsp;Yanjun Wang ,&nbsp;Ran Zhuang ,&nbsp;Yuan Zhang ,&nbsp;Junjie Li ,&nbsp;Jiangang Xie ,&nbsp;Wen Yin","doi":"10.1016/j.yexcr.2025.114686","DOIUrl":"10.1016/j.yexcr.2025.114686","url":null,"abstract":"<div><h3>Background</h3><div>The biogenesis of microRNAs (miRNAs) undergoes substantial alterations in response to various stressors. Drosha, a pivotal regulator of miRNA biogenesis, plays a critical role in cellular responses to external stimuli. The RNA-binding protein HuR is upregulated upon cellular stress. However, under severe or prolonged stress conditions, HuR levels may decline, impairing its protective functions.</div></div><div><h3>Methods</h3><div>To investigate the influence of HuR on miRNA expression, miRNA sequencing was employed to profile expression in IEC-6 intestinal epithelial cells following HuR silencing. Additionally, the effect of HuR overexpression on Drosha expression and activity was assessed. Bioinformatics analyses, biochemical assays, and molecular biology techniques were utilized to elucidate the mechanisms by which HuR interacts with <em>Drosha</em> mRNA, modulating both its translation and transcription.</div></div><div><h3>Results</h3><div>HuR silencing resulted in a significant downregulation of nearly all miRNAs, with no observed impact on piRNA biogenesis. Conversely, HuR overexpression led to increased Drosha expression, regulated through HuR's direct binding to the 3′-UTR of <em>Drosha</em> mRNA. Moreover, HuR indirectly promoted Drosha transcription by elevating c-Myc levels. In a mouse model of thoracic trauma, diminished HuR expression in the intestinal epithelium correlated with reduced Drosha levels, impairing miRNA biogenesis and enhancing apoptosis.</div></div><div><h3>Conclusions</h3><div>These findings underscore the essential role of HuR in the regulation of miRNA biogenesis through Drosha, with implications for stress responses and intestinal injury. The HuR-Drosha axis emerges as a promising therapeutic target for modulating miRNA biogenesis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 1","pages":"Article 114686"},"PeriodicalIF":3.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717831","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}

{"title":"Understanding variability in cell death modes and sensitivity: Potential implications for targeted cancer therapies.","authors":"Magdalena Wegrzyn, Malgorzata Adamiec-Organisciok, Anahit Dawicka, Daniel Fochtman, Seweryn Galecki, Ngoni Magate, Kinga Bartel, Daria Gendosz de Carrillo, Emilia Witek-Zelazny, Magdalena Skonieczna","doi":"10.1016/j.yexcr.2025.114688","DOIUrl":"10.1016/j.yexcr.2025.114688","url":null,"abstract":"<p><p>Cell death is an inseparable mechanism accompanying the individual development of multicellular organisms. In every organism, there must be a constant exchange and regulation of the number of cells in tissues, consisting of the control of their proliferation, inhibition of the cell cycle, or induction of cell death pathways. The proper functioning of the physiological mechanisms of cell death (e.g., apoptotic) determines the maintenance of homeostasis, understood as the internal balance of the body, which directly depends on the appropriate pH levels, osmotic pressure, or concentration of individual chemical compounds. Regulated cell death (RCD) plays an important role in the body's homeostasis, but in case of its disruption, and without control over the regulation of one or more types of cell death, it can cause diseases such as cancer, neurodegeneration, and autoimmune diseases. RCD can take many forms, including apoptosis, necroptosis, or ferroptosis. This review focuses the variability in dominant modes of cell death, sensitivity, and response pathways across different tumor cell lines. Understanding these dynamics is essential for optimizing novel treatment modalities and improving cancer's patient prognosis.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114688"},"PeriodicalIF":3.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764801","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}