Cell Biochemistry and Function最新文献

{"title":"A Tumor Microenvironment-Derived CAF-VEGF Model and Its Application in Biomarker Screening for HCC","authors":"Hao Zheng,&nbsp;Shengwei Tang,&nbsp;Ruida Shi,&nbsp;Yanting Zhu,&nbsp;Xitong Geng,&nbsp;Shuhan Huang,&nbsp;Ruiyu Zhang,&nbsp;Xiaoyu Qu,&nbsp;Hao Wan,&nbsp;Chenshuo Fang,&nbsp;Xin Wang,&nbsp;Ye zhu,&nbsp;Yuhong Feng,&nbsp;Da Huang,&nbsp;Weifan Jiang","doi":"10.1002/cbf.70204","DOIUrl":"10.1002/cbf.70204","url":null,"abstract":"<div>\u0000 \u0000 <p>HCC is a highly vascularized solid tumor that develops rapidly and has a poor prognosis. Previous studies have shown that fibroblasts and angiogenesis in the tumor microenvironment play significant roles in the progression of HCC, and the combined effect of both on HCC is worth exploring. Therefore, we developed the CAF-VEGF prognostic scoring model to assess the prognosis of HCC patients. Single-cell sequencing was done on cancer tissues and nearby normal tissues in the study using data that we downloaded from the GEO database. We used the CellChat and Monocle3 packages to analyze the angiogenesis pathways and differentiation trajectories of fibroblasts. Subsequently, we conducted functional enrichment on fibroblasts. We constructed the CAF-VEGF prognostic model using the COX and LASSO algorithms and evaluated its prognostic value through survival and ROC curves. Based on the prognostic model, we identified key genes through differential expression screening, WGCNA, and PPI network analysis. The conclusions were ultimately validated by expression experiments and functional assays. We found that fibroblasts had a higher infiltration rate in HCC tissues and successfully constructed a CAF-VEGF prognostic model in HCC, proving its effectiveness. Using the CAF-VEGF score, we identified the key molecular markers ESCO2 and WDHD1, both significantly upregulated in HCC cells. Their overexpression may lead to poor prognosis in HCC patients. Additionally, through experiments, we found that both can promote angiogenesis and enhance the proliferation and invasion-migration abilities of HCC cells. This study successfully constructed the CAF-VEGF prognostic model for HCC, and may help improve the prognosis of HCC patients. We also found that the genes WDHD1 and ESCO2 can promote HCC infiltration by regulating angiogenesis, providing insights for future HCC treatment.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147572369","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":"Targeting Prion Protein to Overcome Doxorubicin Resistance in SCLC","authors":"Fatih Çöllü,&nbsp;Hayrettin Kadinşah,&nbsp;Zübeyde Öztel,&nbsp;Berrin Tuğrul,&nbsp;Erdal Balcan","doi":"10.1002/cbf.70201","DOIUrl":"10.1002/cbf.70201","url":null,"abstract":"<div>\u0000 \u0000 <p>Multidrug resistance (MDR) remains a major challenge in small cell lung cancer (SCLC), limiting the efficacy of chemotherapeutics like doxorubicin. This study investigates whether silencing cellular prion protein (PrP), a known MDR-associated molecule, can enhance doxorubicin-induced cell death in Adriamycin-resistant H69AR cells. Quantitative RT-PCR and immunocytochemistry were used to assess the expression of <i>PRNP</i>, <i>CD44</i>, <i>BAX</i>, and <i>BECN1</i> under various treatment conditions, including doxorubicin exposure and PrP knockdown via siRNA. Autophagic activity was evaluated using monodansylcadaverine (MDC) staining. PrP knockdown significantly reduced <i>PRNP</i> expression and modulated <i>CD44</i> mRNA levels, especially during doxorubicin co-treatment. However, CD44 protein levels remained unchanged, suggesting post-transcriptional regulation. <i>BAX</i> expression increased with doxorubicin and siRNA individually, but not in combination, indicating a PrP-independent mechanism. <i>BECN1</i> expression and Beclin-1 protein levels were significantly elevated in all treatment groups, especially in siRNA/doxorubicin combination. MDC staining confirmed increased autophagic vacuole formation in this group, indicating activation of Beclin-1-mediated autophagy. In conclusion, PrP knockdown may sensitize resistant SCLC cells to doxorubicin and promote autophagy. These findings support PrP silencing as a promising strategy to reverse chemoresistance in SCLC.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147527151","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":"Histamine and Pruritus: From Molecular Mechanisms to Clinical Therapy","authors":"Ya-An Lan,&nbsp;Jia-Xi Guo,&nbsp;Min-Hua Yao,&nbsp;Zi-Rui Liao,&nbsp;Yu-Hong Jing","doi":"10.1002/cbf.70199","DOIUrl":"10.1002/cbf.70199","url":null,"abstract":"<div>\u0000 \u0000 <p>Itching is an unpleasant sensory experience that induces the desire to scratch and is clinically divided into histamine-dependent and non-dependent types, with the former being the main clinical type. Its pathogenesis mainly involves mast cell degranulation due to various factors, releasing histamine and causing itching. Histamine, a classical pruritogen, is mainly associated with acute pruritus and is the main endogenous pruritic agent responsible for pruritus in patients with allergic skin diseases after exposure to allergens. In recent years, significant progress has been made in understanding the neurocircuits of histamine-dependent itch from the periphery to the central nervous system. This review focuses on the neurocircuits of histamine-dependent itch, summarizes the major recent advances in this field, and explores the clinical diagnosis and therapy of histamine-dependent pruritus based on basic neuroscience findings. By delving into the mechanisms of histamine in the generation, transmission, and processing of itch sensation, this article provides a better entry point and theoretical basis for the treatment of pruritus, especially histamine-related pruritus, and helps to develop more effective anti-pruritic drugs in the future to improve patients' quality of life.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509649","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":"Molecular and Cellular Mechanisms of Sarcopenia: Integrating Fiber-Type Remodeling, Contractile Protein Dynamics, and Systemic Regulatory Pathways","authors":"Nikam Rutuja Dilesh,&nbsp;Divyansh Khatri,&nbsp;Richa Shrivastava,&nbsp;Sapana Kushwaha","doi":"10.1002/cbf.70194","DOIUrl":"10.1002/cbf.70194","url":null,"abstract":"<div>\u0000 \u0000 <p>Sarcopenia is an age-associated skeletal muscle disorder characterized by progressive declines in muscle mass, strength, and functional performance. A central feature of sarcopenic remodeling is the preferential loss of fast-twitch (Type II) fibers and alterations in contractile protein composition, leading to reduced force generation and impaired muscle quality. Maintenance of skeletal muscle function depends on the integrity of the contractile apparatus, including myosin heavy chain isoforms, titin, actin, troponin, and associated structural proteins, which undergo quantitative and qualitative changes with aging. Multiple aging-related mechanisms including telomere attrition, epigenetic remodeling, mitochondrial dysfunction, ionic dyshomeostasis, hormonal alterations, and chronic low-grade inflammation converge on fiber-type regulation and sarcomeric stability. These upstream processes impair satellite cell renewal, disrupt excitation–contraction coupling, accelerate proteolysis of contractile proteins, and promote maladaptive fiber-type transitions. Ankyrins and muscle ankyrin repeat proteins (MARPs) further modulate sarcomere organization, mechanotransduction, and adaptive stress signaling. Age-related dysregulation of ankyrin–contractile protein interactions compromises structural stability and regenerative capacity, contributing to muscle weakness and frailty. Viewing sarcopenia through the integrated framework of fiber-type plasticity, contractile protein dynamics, and ankyrin-mediated regulation provides a unifying mechanistic perspective that links systemic aging processes to structural muscle decline. This approach highlights potential biomarkers and therapeutic targets for preserving muscle function in aging populations.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472767","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":"Unveiling the 12-Hour Ultradian Rhythm: Biological Foundations, Mechanistic Insights, and Potential Applications","authors":"Jiayi Song,&nbsp;Chuyao Wang,&nbsp;Hongyu Li,&nbsp;Ting Wang,&nbsp;Xinwei Jiao","doi":"10.1002/cbf.70195","DOIUrl":"10.1002/cbf.70195","url":null,"abstract":"<div>\u0000 \u0000 <p>The ~12-h ultradian rhythm (circasemidian) represents an evolutionarily conserved temporal architecture that complements the canonical 24-h circadian clock. Over the past 5 years, mounting evidence has revealed its ubiquity across biological kingdoms, from tidal marine organisms and cyanobacteria to plants, microbiomes, and mammals, including humans, manifesting as intrinsic oscillations in gene expression, metabolism, and behavior that often persist independently of circadian control. In mammals, this rhythm is driven by a cell-autonomous oscillator centered on the XBP1s (X-box binding protein 1)/IRE1α (Inositol requiring enzyme 1 alpha) axis, orchestrating endoplasmic reticulum stress responses and lipid homeostasis through negative feedback regulation, further reinforced by metabolic coupling and bidirectional crosstalk with circadian pathways. Functionally, 12-h oscillations act as a secondary temporal layer that ensures bimodal photostatic and energetic homeostasis, synchronizing multi-organ physiology across the day–night transition. Pathologically, disruption of this rhythm contributes to metabolic syndromes (e.g., NAFLD (non-alcoholic fatty liver disease), diabetes), neuropsychiatric disorders (e.g., schizophrenia), and age-related dysfunctions, particularly within ocular and immune systems. Despite accumulating correlative and model-based evidence, causal mechanisms remain insufficiently defined, and human data are limited. Future work integrating multi-omics chrono profiling, comparative genomics, and clinical chronotherapeutic trials will be critical to delineate this semidiurnal oscillator's molecular architecture and translational potential, thereby advancing precision chrono medicine and expanding the current paradigm of biological timing.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472807","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":"Comprehensive Overview of Therapeutic Strategies in Colon Cancer: Chemotherapy, Targeted Therapy, and Immunotherapy","authors":"Seerwan Hamadameen Sulaiman,&nbsp;Hemn A. H. Barzani,&nbsp;Rebaz Anwar Omer,&nbsp;Zanco Hassan Jawhar,&nbsp;Ali Abdulhameed Mohammedsaeed","doi":"10.1002/cbf.70196","DOIUrl":"10.1002/cbf.70196","url":null,"abstract":"<div>\u0000 \u0000 <p>Colon cancer remains a leading global health challenge driven by substantial molecular heterogeneity, complex carcinogenic pathways, and the persistent emergence of therapeutic resistance. This review provides a comprehensive and integrative synthesis of contemporary treatment strategies spanning conventional chemotherapy, molecularly targeted agents, and immunotherapy while contextualizing them within the biological mechanisms that shape therapeutic response. We dissect the mechanistic underpinnings and clinical performance of foundational regimens such as FOLFOX, FOLFIRI, and CAPOX, and analyze how key driver alterations, including RAS/RAF mutations, HER2 amplification, MSI/MMR status, and VEGF-mediated angiogenesis, influence disease progression and therapeutic selection. In addition, we analyze shared resistance pathways and the mechanistic rationale supporting rational combination strategies, including BRAF/EGFR/MEK blockade, HER2-directed dual targeting, and PD-1/PD-L1–based combinations aimed at overcoming immune exclusion in MSS tumors. Emerging advances such as KRAS G12C inhibitors, multi-kinase angiogenesis modulators, antibody–drug conjugates, ribosome biogenesis inhibitors, AI-guided therapeutic algorithms, and ctDNA-based monitoring are also discussed. By integrating mechanistic insights with clinical evidence, this review offers a structured framework to better understand current treatment paradigms and future directions in biomarker-driven precision therapy for colon cancer.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472765","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":"From Endoplasmic Reticulum Homeostasis to Cardiac Protection: The Role of UFMylation in Cardiovascular Diseases","authors":"Liuhong Chen,&nbsp;Wenyuan Xu,&nbsp;Xishun Zhou,&nbsp;Chenran Ren,&nbsp;Fang Liu,&nbsp;Xi Zeng","doi":"10.1002/cbf.70198","DOIUrl":"10.1002/cbf.70198","url":null,"abstract":"<div>\u0000 \u0000 <p>The development and progression of cardiovascular diseases (CVDs) are closely linked to an imbalance in endoplasmic reticulum homeostasis. UFMylation, a recently identified ubiquitin-like post-translational modification, plays a crucial role in maintaining cellular homeostasis by regulating substrate protein functions through a unique enzymatic cascade. Accumulating evidence has demonstrated that UFMylation exerts complex regulatory effects on the pathogenesis of atherosclerosis, primarily by modulating endothelial function, macrophage foam cell formation, and inflammasome activation. Furthermore, UFMylation of the calcium-regulating protein SPCA1 disrupts calcium homeostasis in hypertrophic cardiomyopathy. Conversely, UFMylation also exhibits protective roles; for instance, it prevents pathological cardiac remodeling in heart failure by maintaining endoplasmic reticulum function via its E3 ligase, UFL1. Accordingly, this review systematically summarizes these multifaceted protective mechanisms of UFMylation in CVDs. We also explore potential therapeutic strategies targeting UFMylation, discussing its promise as a CVD biomarker and the opportunities and challenges in developing UFMylation agonists. In-depth research in this field is expected to provide novel theoretical foundations and precise intervention targets for the prevention and treatment of CVDs.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472776","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":"Regulation of Choroid Plexus Bicarbonate Transporters Following Intraventricular Hemorrhage in Mice","authors":"Laura Øllegaard Johnsen,&nbsp;Rasmus Herløw,&nbsp;Rasmus West Knopper,&nbsp;Thomas Beck Lindhardt,&nbsp;Brian Hansen,&nbsp;Helle Hasager Damkier","doi":"10.1002/cbf.70197","DOIUrl":"10.1002/cbf.70197","url":null,"abstract":"<p>Posthemorrhagic hydrocephalus is a severe complication to intraventricular hemorrhage. The condition results in enlarged brain ventricles and increased intracranial pressure due to accumulation of cerebrospinal fluid (CSF). In this study, two mouse models of intraventricular hemorrhage were investigated: injection of lysed red blood cells (LRBC) and injection of autologous full blood. CSF secretion and ventricular volume were assessed using ventriculo-cisternal perfusion and magnetic resonance imaging (MRI), while molecular and biochemical responses were analyzed by immunoblotting, RT-qPCR, flame photometry, and blood-gas measurements. LRBC injection induced a transient change in choroid plexus bicarbonate transporter expression, as the protein-abundance of Ncbe, a basolateral sodium-bicarbonate transporter, was reduced by 23% after 24 h but increased by 17% after 48 h. Injection with full blood transiently increased mRNA levels of the basolateral sodium-bicarbonate transporter NBCn1 and Ncbe without altering protein expression. The luminal electrogenic sodium: bicarbonate transporter, NBCe2, was unaffected both at the RNA and protein level. Both models were validated using ventriculo-cisternal perfusion demonstrating an increase in CSF volume by 70% in the IVH model after 24 h and 73% in the LRBC model after 3 days. No effect on secretion rate of CSF was detected. Additionally, in the LRBC model MRI was used to assess the time-course of brain ventricle size following hemorrhage. Here, an overall volume increase of 30% was found in the hemorrhage-induced mice compared to the control. These results demonstrate that both LRBC and full-blood injections can induce ventricular enlargement in mice, but through different molecular responses. Neither model reproduced sustained CSF hypersecretion, underscoring that murine models of intraventricular hemorrhage display a milder form of pathophysiology compared to e.g. rats.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Briefing on Nitric Oxide a Signal Molecule in Cancer Metastasis and Therapeutic Target","authors":"Seema Kumari","doi":"10.1002/cbf.70191","DOIUrl":"10.1002/cbf.70191","url":null,"abstract":"<div>\u0000 \u0000 <p>Nitric oxide (NO) is an important signaling molecule in maintaining normal physiological processes like blood flow, neurotransmission and immune regulation. In cancer, it exhibits a dual role in context-dependent mechanism. At low levels, it activates angiogenesis, migration and tumor promotion; on the other hand, with an increase in concentration, it promotes apoptosis and has an anti-metastatic effect. Hence, regulated levels of NO are required to maintain normal hemostasis. NO has temporal and spatial regulation as its pro- and anti-metastatic effects are decided by the tumor stage, tumor microenvironment, and nitric oxide synthase isoforms expression. NO regulates EMT markers like upregulation of Snail, Twist, and ZEB1 (pro-EMT factors and downregulation of E-cadherin. NO also regulates the crosstalk between signaling factors, such as TGF-β, Wnt/β-catenin and NF-κB; during EMT and hypoxia-induced angiogenesis. NO promotes immunosuppression and metastasis by interacting with tumor-associated macrophages and myeloid-derived suppressor cells, which express iNOS. NO activates cancer promotion pathways like NF-κB, upregulates pro-metastatic genes (MMPs, cytokines), PI3K/Akt/mTOR and p53/Nrf2, along with regulating non-coding RNAs. Thus, NO is a potential target in cancer therapeutics and reviews focus on the new advancements using NO as a potential biomarker and therapeutic agent.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354132","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":"Disruption of Cytoskeleton Induces Physiologically and Morphologically Dysfunctional Mitochondria in B-ALL Cells","authors":"Bhanu Priya Awasthi,&nbsp;Bhanupriya Tanwar,&nbsp;Akshi Shree,&nbsp;Sumedha Saluja,&nbsp;Jayanth Kumar Palanichamy,&nbsp;Sameer Bakhshi,&nbsp;Archna Singh","doi":"10.1002/cbf.70190","DOIUrl":"10.1002/cbf.70190","url":null,"abstract":"<div>\u0000 \u0000 <p>The interaction of cellular organelles is crucial for maintaining intracellular homeostasis, particularly highlighting the impact of the cytoskeleton on mitochondrial dynamics. The aim of our study is to find direct molecular connections between cytoskeletal disturbance and mitochondrial failure which are inadequately characterized particularly in B-ALL. We investigated the effects of cytoskeleton inhibition on mitochondria in B-ALL using Pironetin (an alpha-tubulin inhibitor) and Latrunculin B (an actin inhibitor). Our findings indicate that these inhibitors caused mitochondrial fragmentation, characterized by smaller, rounder mitochondria with disordered cristae, increased Drp1 expression (fission protein), and decreased Mfn 1/2 and OPA 1 (fusion proteins) together with significantly modified the expression of essential mitochondrial transporters, such as VDAC and ANT2. These alterations were linked to increased mitochondrial membrane depolarization &amp; mitochondrial reactive oxygen species and gradual mtDNA depletion, indicative of impaired oxidative phosphorylation (increased non-mitochondrial oxygen consumption, decreased mitochondrial reserve capacity) and diminished mitochondrial functionality. These mitochondrial alterations indicate that communication between the cytoskeleton and mitochondria is essential for preserving mitochondrial homeostasis. This study potentially enhances our understanding of how cancer cells modulate mitochondrial function during progression or therapeutic interventions.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321409","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}