Frontiers in Molecular Biosciences最新文献

{"title":"Glucan exopolysaccharide from <i>Enterococcus hirae</i> OL616073 alleviates oxidative stress and extends lifespan in different model systems.","authors":"Uma Rani Potunuru, P Padmapriya, Balasubramanian Chellammal Muthubharathi, Bargavi A Meenachi, Raksha Goswami, Palanisamy Bruntha Devi, Anjali Mohan, Krishnaswamy Balamurugan, Arunkumar Dhayalan, Digambar Kavitake, Prathapkumar Halady Shetty","doi":"10.3389/fmolb.2026.1901988","DOIUrl":"10.3389/fmolb.2026.1901988","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to evaluate the oxidative stress alleviating potential of glucan exopolysaccharide (EPS) using <i>in vitro</i> (biochemical and cell culture) and <i>in vivo Caenorhabditis elegans</i> model systems.</p><p><strong>Methods: </strong>The <i>in vitro</i> antioxidant potential of EPS from <i>Enterococcus hirae</i> OL616073 of food origin was evaluated using reducing power, ferric-reducing antioxidant power (FRAP) assay, and 2,2-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical-scavenging activity assays. The antioxidant effect of EPS was also evaluated in <i>C. elegans</i> (wild type Bristol N2), a simple multi-cellular eukaryotic model via survival assay, gene expression, DCF-DA staining, reproduction, and pharyngeal pumping assay. Finally, the ROS scavenging activity of EPS was investigated in human colon cancer cells (Caco-2 cell line) by DCF-DA staining and flow cytometry.</p><p><strong>Results and discussion: </strong>The <i>in vitro</i> assays showed the significant antioxidant activity of EPS as evidenced by reducing power, FRAP, and ABTS radical-scavenging activity. In <i>C. elegans</i>, EPS treatment (150 and 300 μg/mL) significantly extended the lifespan of wild-type (Bristol N2) <i>C. elegans</i> (∼1.21% and ∼0.83%) compared to control. EPS treatment (150 μg/mL) resulted in increased egg-laying capacity and little change in the pharyngeal pumping rate of <i>C. elegans</i> over five consecutive days. In addition, pre-, post-, and co-treatment of EPS (150 μg/mL) in the presence or absence of H₂O₂ (1 mM) showed a reduction in ROS generation. Similarly, in the colorectal cancer cell line (Caco-2), high basal intracellular ROS levels were reduced with increasing concentration of EPS via an increase in intracellular antioxidant enzymes.</p><p><strong>Conclusion: </strong>EPS from <i>E. hirae</i> OL616073 of food origin exhibited significant antioxidant potential across diverse model systems. These findings highlight its potential as a natural antioxidant ingredient for applications in functional foods, nutraceuticals, and pharmaceutical formulations.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1901988"},"PeriodicalIF":4.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896783","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":"Impact of oxidative stress on malignant tumor progression and emerging therapeutic strategies.","authors":"Xudong Feng, Guicai Liang, Jingjing Sun, Zhiqiang Wang, Tao Li, Yang Fu, Wen Deng, Xiuying Li, Jie Luo, Ping Jin, Chunlei Ge, Rongqing Li","doi":"10.3389/fmolb.2026.1916698","DOIUrl":"10.3389/fmolb.2026.1916698","url":null,"abstract":"<p><p>Oxidative stress, driven by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, plays a pivotal role in cancer biology. While persistent, moderately elevated ROS levels can promote genomic instability, tumor progression, and immune evasion, excessive ROS accumulation can overwhelm antioxidant defenses and trigger cancer cell death. Despite promising preclinical findings, clinical translation remains a challenge because of the context-dependent effects of ROS. A deeper understanding of oxidative stress regulation may lead to the development of novel precision medicine strategies, optimizing cancer therapies while minimizing adverse effects. This review highlights the concentration-dependent effects of oxidative stress in tumorigenesis, focusing on its impact on DNA damage, metabolic reprogramming, and immune modulation. We discuss recent advancements in ROS-targeting strategies, including pro-oxidant therapies that exploit redox vulnerabilities in cancer cells and antioxidant-based approaches aimed at mitigating oxidative stress-driven resistance to treatment. Moreover, we examine the interplay between oxidative stress and the tumor microen-vironment, emphasizing its influence on immune surveillance and therapeutic responses. This re-view provides insights into ROS-targeting interventions and their potential in oncologic treatment paradigms.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1916698"},"PeriodicalIF":4.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896864","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":"Nanozymes for extracellular matrix and cell sheet engineering: biomedical potential and complementary enzymatic strategies.","authors":"Soon Mo Choi, Sum Mi Zo, Ankur Sood, Sung Soo Han","doi":"10.3389/fmolb.2026.1900627","DOIUrl":"10.3389/fmolb.2026.1900627","url":null,"abstract":"<p><p>Cell sheet engineering has emerged as a scaffold-free biofabrication strategy that preserves intrinsic cell-cell and cell-extracellular matrix interactions, demonstrating significant translational potential in regenerative medicine, including cardiac patches, cartilage and skin reconstruction, and corneal transplantation. Despite these advances, thick or multilayered cell sheets remain constrained by diffusion related hypoxia, accumulation of reactive oxygen species, ECM destabilization, and insufficient mechanical reinforcement, all of which interact to compromise long term structural integrity. Rather than providing a conventional survey of recent developments, this conceptual integration review reframes these limitations as a coupled reaction-diffusion-mechanics problem. We examine how redox imbalance and structural insufficiency form a self-reinforcing failure network in thick scaffold-free constructs and propose a reciprocal dual-axis catalytic framework to address this instability. Nanozymes, through catalase-, peroxidase-, and superoxide dismutase-like catalytic activities, regulate oxidative stress, alleviate hypoxic amplification, and establish a permissive redox microenvironment that sustains cell viability and ECM synthesis. In parallel, immobilized enzyme systems facilitate collagen crosslinking and protease modulation, thereby reinforcing ECM architecture and enhancing tensile and shear resilience at the network level. Although nanozyme-based redox regulation and enzyme-mediated structural reinforcement have been extensively explored in oncology, antioxidant therapeutics, and industrial catalysis, their coordinated implications for scaffold-free cell sheet engineering have not been systematically integrated. By articulating a reciprocal dual-axis framework linking redox stabilization with biomechanical maturation, this review provides a systems-level design logic for improving thick cell sheet stability. Finally, we extend this catalytic paradigm beyond regenerative medicine to high-density sheet-like biofabrication systems, including cultured meat and cultured leather, positioning the framework as a transferable engineering principle across emerging biofabrication industries.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1900627"},"PeriodicalIF":4.4,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13538886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886362","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":"Novel GLA variant (c.752A>C; p.Glu251Ala) identified in a patient with Fabry cardiomyopathy and familial segregation.","authors":"Ting Zhang, Sulan Huang, Fan Huang","doi":"10.3389/fmolb.2026.1828669","DOIUrl":"10.3389/fmolb.2026.1828669","url":null,"abstract":"<p><strong>Background: </strong>Fabry disease (Anderson-Fabry disease,FD) is an X-linked lysosomal storage disorder caused by variants in GLA, resulting in α-galactosidase A (α-Gal A) deficiency and accumulation of globotriaosylsphingosine (lyso-Gb3), with frequent cardiac involvement.</p><p><strong>Case summary: </strong>A 53-year-old man presented with exertional chest tightness and dyspnea. Electrocardiography and echocardiography demonstrated marked left ventricular hypertrophy. Cardiac magnetic resonance revealed diffuse hypertrophy with extensive subendocardial late gadolinium enhancement. ^99mTc-pyrophosphate scintigraphy showed minimal myocardial uptake, arguing against transthyretin cardiac amyloidosis. Biochemical testing showed markedly reduced α-Gal A activity and elevated lyso-Gb3 levels. Whole-exome sequencing identified a previously unreported GLA variant (NM_000169.3:c.752A>C; p.Glu251Ala), which was confirmed by Sanger sequencing and detected in multiple family members. The variant is currently classified as a variant of uncertain significance (VUS). Familial analysis demonstrated a segregation pattern consistent with X-linked inheritance.</p><p><strong>Conclusion: </strong>We report a novel GLA variant associated with biochemical abnormalities and familial segregation consistent with FD. These findings support a potential role of this variant in Fabry cardiomyopathy and expand the mutational spectrum of GLA, although its pathogenicity requires further validation.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1828669"},"PeriodicalIF":4.4,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13537968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886491","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":"Functional characterisation of PREL-1 and PREL-3 proteins as putative intramitochondrial phospholipid transporters governing homeostasis and organismal health in <i>Caenorhabditis elegans</i>.","authors":"Vijay Aditya Mavuduru, Lavanya Vadupu, Kiruthiga Shankar Kumar, Naga Bhushana Rao Karampudi, Writoban Basu Ball","doi":"10.3389/fmolb.2026.1892600","DOIUrl":"10.3389/fmolb.2026.1892600","url":null,"abstract":"<p><strong>Introduction: </strong>Mitochondrial phospholipids are crucial for maintaining structure and function; however, their roles and transport pathways are not fully understood in a multicellular model organism. In this study, we examined two putative <i>Caenorhabditis elegans</i> proteins, B0334.4 (PREL-1) and F15D3.6 (PREL-3), thought to be involved in intramitochondrial phospholipid transport.</p><p><strong>Methods: </strong><i>In-silico</i> molecular docking analysis was performed to predict phospholipid binding specificity of PREL-1 and PREL-3. RNA interference (RNAi) was used to knockdown the expression of these proteins in <i>C. elegans.</i> Upon knockdown, development, lifespan, reproduction, locomotion, stress response, and mitochondrial phospholipid composition were analysed.</p><p><strong>Results: </strong>Docking studies predicted that phosphatidic acid (PA) preferentially binds to PREL-1 compared to PREL-3. Mitochondrial profiling revealed loss of mitochondrial phospholipid homeostasis upon RNAi knockdown. This resulted in mitochondrial dysfunction leading to impaired reproduction, respiration, locomotion, and elevated ROS levels in worms lacking these phospholipid transporters.</p><p><strong>Conclusion: </strong>Our findings support the role of PREL-1 and PREL-3 proteins in mitochondrial phospholipid homeostasis and suggest their function as PRELI- family phospholipid transporters. This study demonstrates the importance of these phospholipid transporters in mitochondrial function, growth, lifespan, and organism physiology.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1892600"},"PeriodicalIF":4.4,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879486","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":"Lactylation in sepsis-associated acute kidney injury: regulatory mechanisms and therapeutic prospects.","authors":"Jiahui Zheng, Boyang Zheng, Qun Liang","doi":"10.3389/fmolb.2026.1899336","DOIUrl":"10.3389/fmolb.2026.1899336","url":null,"abstract":"<p><strong>Introduction: </strong>Sepsis-associated acute kidney injury (SA-AKI) is a prevalent, life-threatening sepsis complication with high mortality, prolonged organ support dependence, and scarce targeted therapies. Beyond being an anaerobic glycolysis byproduct, lactate serves as a critical circulating carbon source, mitochondrial fuel, redox regulator, signaling molecule, and lysine lactylation (Kla) substrate. Its multifaceted functions are vital to SA-AKI pathogenesis, which involves systemic lactate overload, impaired lactate clearance, renal metabolic reprogramming, and abnormal immune activation.</p><p><strong>Methods: </strong>This review synthesizes up-to-date evidence to systematically elucidate lactate and Kla mechanisms in SA-AKI. We hierarchically integrate findings from systemic sepsis metabolism and renal tubular lactate handling to cell-specific Kla modifications, aiming to clarify their distinct roles in SA-AKI progression.</p><p><strong>Results: </strong>Specific Kla sites (H3K18la, Fis1 K20la, LDHB K156la, Ezrin K263la, HMGB1 lactylation, ALDH2 K68la) mediate SA-AKI pathologies including mitochondrial dysfunction, tubular death, endothelial injury, and cGAS-STING/NLRP3-neutrophil extracellular trap activation. Lactate accumulation, acidosis, transport, oxidation, metabolic routing, and Kla are mechanistically distinct rather than uniformly harmful. Lactate/pyruvate metabolism exerts context-dependent injurious or adaptive effects across kidney disease models, modulated by cell type, injury phase, and metabolic reserve.</p><p><strong>Discussion: </strong>Lactate- and Kla-targeted strategies are promising for SA-AKI treatment yet require rigorous clinical validation. Blood lactate level and clearance are reliable clinical prognostic biomarkers, whereas Kla signatures remain investigational. Balanced understanding of lactate-Kla biology will refine precision diagnostic and therapeutic strategies for SA-AKI, advancing translational clinical application.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1899336"},"PeriodicalIF":4.4,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13536897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879548","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":"Targeting ferroptosis and mitochondrial ROS: organoprotective mechanisms of anesthetic conditioning in liver transplantation.","authors":"Junming Li, Weijun Zeng, Juan Yang","doi":"10.3389/fmolb.2026.1901963","DOIUrl":"10.3389/fmolb.2026.1901963","url":null,"abstract":"<p><p>Liver transplantation is the definitive treatment for advanced liver failure, yet ischemia-reperfusion injury (IRI) remains a major challenge-particularly for marginal, steatotic, or donation-after-circulatory-death (DCD) grafts. While oxidative stress and inflammation are long-recognized contributors to IRI, this review focuses on two tightly linked, mechanistically specific pathways: ferroptosis and mitochondrial reactive oxygen species (ROS). Together, these pathways convert reperfusion-associated metabolic stress into injury of hepatocytes, endothelium, and bile ducts. Anesthetic preconditioning has gained interest as a modulator of this injury cascade. Volatile anesthetics, alongside propofol and dexmedetomidine, show experimental efficacy in reducing IRI by stabilizing mitochondria, regulating redox status, preserving GPX4(Glutathione Peroxidase 4)/SLC7A11(Solute Carrier Family 7 Member 11)-mediated antioxidant capacity, limiting lipid peroxidation, and dampening innate immune responses. However, clinical translation is limited by heterogeneity in experimental models, variability in anesthetic regimens, overreliance on non-specific oxidative stress markers, and a lack of validated ferroptosis-related endpoints in human studies. In summary, ferroptosis and mitochondrial ROS provide a cohesive mechanistic framework for graft vulnerability at reperfusion. To advance this field, future clinical studies should move beyond general oxidative stress assessments toward biomarker-driven approaches-integrating ferroptosis-specific markers and mitochondrial function tests. Coupling these with risk stratification of donor livers based on biochemical profiles, and tracking clinically meaningful outcomes, will enable precision strategies to mitigate IRI. This review underscores the need for targeted mechanistic validation to translate anesthetic conditioning into effective clinical organ protection.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1901963"},"PeriodicalIF":4.4,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13535284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879500","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":"MicroRNA signatures in inflammatory dental tissues: biomarkers and molecular mechanisms.","authors":"Dandan Shao, Zhenyu Yao","doi":"10.3389/fmolb.2026.1881450","DOIUrl":"10.3389/fmolb.2026.1881450","url":null,"abstract":"<p><p>Inflammatory immune responses in the dental pulp are shaped by interacting cellular and molecular processes, and microRNAs (miRNAs) are important post-transcriptional regulators. However, an integrated understanding of how miRNA networks orchestrate the balance between pulpitis progression and tissue repair remains incomplete. This review examines the differential expression profiles of miRNAs in inflamed dental pulp, and evaluates their potential as adjunctive biomarkers of pulpitis status. We also summarize how miRNAs regulate key inflammatory signaling cascades, including the TLR/NF-κB, mitogen-activated protein kinase, and cGAS-STING pathways, and discuss their integration within broader epigenetic crosstalk networks involving lncRNAs and circRNAs. We further analyze how the inflammatory microenvironment and physicochemical stresses alter the osteogenic/odontogenic differentiation potential of dental pulp stem cells through miRNA-dependent regulation. We then assess the translational prospects of exosome-delivered miRNAs as cell-free therapeutics and highlight unresolved challenges in sampling feasibility, donor heterogeneity, delivery specificity, and clinical validation. By synthesizing evidence on miRNA regulatory networks in pulpal inflammation and regeneration, this review provides a framework for evaluating miRNA-based diagnostic tools and targeted therapies for pulpitis.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1881450"},"PeriodicalIF":4.4,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13530013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873615","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":"The function of phosphoglycerate mutase 1 (PGAM1) and its role in diseases.","authors":"Aihong Peng, Junqin Li, Huifang Liang, Yuanjun Yao, Kaiming Zhang","doi":"10.3389/fmolb.2026.1842545","DOIUrl":"10.3389/fmolb.2026.1842545","url":null,"abstract":"<p><p>Phosphoglycerate mutase 1 (PGAM1) is a pivotal metabolic enzyme during the process of glycolysis, catalyzing the interconversion between 3-phosphoglycerate and 2-phosphoglycerate. PGAM1 is mainly involved in cellular energy metabolism and biosynthesis, it is generally upregulated in numerous human cancers and promotes cell proliferation, invasion, and drug resistance. It serves as a significant biomarker for tumor diagnosis and a potential therapeutic target. In this paper, the basic structure and functions of PGAM1 and its family members, metabolic, non-metabolic activity and the regulatory mechanisms of PGAM1 and its correlation with diseases, as well as the latest progress of PGAM1 inhibitors in tumor diagnosis and treatment are introduced, aiming to provide new ideas for the targeted therapy of related diseases.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1842545"},"PeriodicalIF":4.4,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864256","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":"Glucosidase GANAB drives colorectal cancer progression through Wnt signaling and is modulated by lncRNA FIRRE.","authors":"Yajie Wang, Wenjun Li, Qian Hua, Zhengyang Li, Miao Jiang","doi":"10.3389/fmolb.2026.1820992","DOIUrl":"10.3389/fmolb.2026.1820992","url":null,"abstract":"<p><strong>Background: </strong>The goal of this study is to investigate the expression pattern of GANAB in colorectal cancer and the role behind it.</p><p><strong>Methods: </strong>In order to study the expression level of GANAB in the tissue of colorectal cancer, we used quantitative real-time PCR and immunohistochemistry. In the aspect of biological function, we study it through the experimental models. The molecular mechanism is clarified by RNA pull-down and RNA stability assays. Student's t-tests and one-way ANOVA are used for data analysis.</p><p><strong>Results: </strong>Analysis of tissue microarrays and Colorectal cancer (CRC) cell lines revealed elevated GANAB expression in tumors compared to normal counterparts. Increased GANAB levels were linked to enhanced cell migration, invasion, and proliferation, and correlated with metastatic potential and unfavorable patient outcomes. Functional enrichment studies indicated that GANAB-associated genes participate in the Wnt/β-catenin signaling pathway. Immunohistochemistry confirmed positive correlations between GANAB and both c-Myc and β-catenin. The oncogenic function of GANAB was shown to rely on Wnt pathway activation. Additionally, lncRNA FIRRE, known to be oncogenic in CRC, was found to physically interact with GANAB mRNA <i>via</i> RNA pull-down assays. FIRRE enhances GANAB mRNA stability through direct binding.</p><p><strong>Conclusion: </strong>Our study demonstrates that GANAB exerts oncogenic effects in CRC by binding directly to lncRNA FIRRE, thereby stabilizing GANAB mRNA and activating the Wnt/β-catenin pathway through nuclear accumulation of β-catenin.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"13 ","pages":"1820992"},"PeriodicalIF":4.4,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13526586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864248","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}