DNA and cell biology最新文献

{"title":"SUMOylation in Neural Health and Disease: From Cellular Homeostasis to Neurodegeneration.","authors":"Ghaleb Oriquat, Ihsan K Jasim, Tushar B Gajjar, Malathi Hanumanthayya, Israa Abdulhameed Ahmad, Gunjan Singh, Laxmidhar Maharana, Neeraj Bainsal","doi":"10.1177/10445498261444640","DOIUrl":"https://doi.org/10.1177/10445498261444640","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDDs) represent a growing global health burden, particularly in aging populations. These disorders primarily affect neurons and are characterized by progressive neuronal dysfunction and loss within specific regions of the central nervous system. Major NDDs include Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, multiple sclerosis, and stroke. Although each disorder exhibits distinct genetic backgrounds and pathological protein aggregates, they share common pathogenic mechanisms, including chronic neuroinflammation, impaired autophagy and mitophagy, disrupted proteostasis, telomere instability, and epigenetic alterations. A hallmark feature across NDDs is the accumulation of misfolded proteins, leading to synaptic dysfunction and neuronal degeneration. Small ubiquitin-like modifiers (SUMOs) are a family of ∼100 amino acid proteins, including SUMO1 and the closely related SUMO2/3 isoforms. SUMOylation is a dynamic posttranslational modification that regulates protein function through the covalent attachment or removal of SUMO moieties. This reversible process is mediated by SUMO-specific E1 activating, E2 conjugating, and E3 ligating enzymes and is counterbalanced by SUMO/Sentrin-specific proteases. The SUMOylation status of target proteins depends on the tightly controlled balance between conjugation and deconjugation systems. Acting as a molecular switch, SUMOylation modulates diverse cellular processes such as DNA damage repair, RNA metabolism, transcriptional regulation, and protein quality control, all of which are essential for maintaining cellular homeostasis. Accumulating evidence links dysregulated SUMOylation to the pathogenesis of multiple neurological disorders, including polyglutamine and synucleinopathies. SUMOylation influences neuroinflammation, oxidative stress, protein aggregation, neuroangiogenesis, ischemic injury, and demyelination. This review highlights recent advances in understanding the role of SUMOylation in NDDs and explores its potential as a promising therapeutic target.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"10445498261444640"},"PeriodicalIF":2.6,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Midbody Remnants as Signaling Centers in Cell Fate Determination and Tumorigenesis.","authors":"Hongbin Li, Xiaoli Ma, Jing Liang, Kai Xue, Wengui Shi, Wanying Lang","doi":"10.1177/10445498261448093","DOIUrl":"https://doi.org/10.1177/10445498261448093","url":null,"abstract":"<p><p>During final cell division, the cleaved midbody is either released or asymmetrically retained as a midbody remnant (MBR). MBRs play critical roles in cell communication, signal transduction, and translation regulation, influencing cellular fate. Here, we synthesize their functions as RNA-processing granules, polarity regulators, and signaling platforms, emphasizing their role in primary cilia formation. In polarized epithelial cells, the MBR moves along the apical surface to the centrosome, delivering membrane components to permit ciliogenesis. In ductal carcinoma cells, MBR-localized Shc1-binding protein (SHCBP1) interacts with TBC1 domain family member 30 (TBC1D30 to antagonize Ras-related protein Rab-8 (Rab8) GTPase activity, blocking MBR-centrosome proximity and silencing ciliogenesis. Beyond ciliary regulation, MBRs integrate Wnt, PDGF, TGF-<i>β</i>, and genomic stability networks, acting as dynamic signaling hubs during cancer development. Regarding therapeutic strategies targeting MBRs, High SHCBP1 expression correlates with ciliary loss and poor prognosis in breast, pancreatic, and cholangiocarcinoma. Targeting the SHCBP1/Rab8 axis to restore ciliogenesis by reestablishing MBR-centrosome proximity offers a potential therapeutic strategy. In addition, secreted MBRs are enriched in signaling components and transcripts, serving as intercellular carriers of oncogenic cargoes and promising liquid biopsy biomarkers. In summary, by tracing MBRs from their postmitotic origin to their pathogenic roles, we highlight vulnerabilities within MBR regulatory networks and provide novel insights for cancer therapeutics.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"10445498261448093"},"PeriodicalIF":2.6,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147824947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLFN11 Enhances PARPi Sensitivity in Ovarian Cancer via Ubiquitin-Mediated Stabilization.","authors":"Minjie Liu, Hongfeng Li, Fang Zhang, Jia Bian, Laifu Fang","doi":"10.1177/10445498261422919","DOIUrl":"10.1177/10445498261422919","url":null,"abstract":"<p><p>Schlafen family member 11 (<i>SLFN11</i>), implicated in cancer drug resistance, may improve poly(ADP-ribose) polymerase inhibitor (PARPi) efficacy. This study investigates <i>SLFN11</i>'s role in epithelial ovarian cancer (EOC) progression and its influence on PARPi sensitivity, particularly in <i>BRCA</i>-wild-type contexts, with a focus on its emerging function in proteostasis regulation. <i>SLFN11</i> expression in EOC and adjacent tissues was evaluated via immunohistochemistry, quantitative polymerase chain reaction (PCR), and Western blot. Functional assays-including cell viability, transwell migration, wound healing, and colony formation-assessed <i>SLFN11</i>'s effects on SKOV3 cells (<i>BRCA</i>-wild-type) proliferation and invasiveness. PARPi sensitivity in SKOV3 cells with <i>SLFN11</i> knockdown or overexpression (OE) was tested using Cell Counting Kit (CCK)-8 and Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assays. Protein stability and ubiquitination levels of <i>PARP1/2</i> were analyzed as the central mechanism. <i>SLFN11</i> mRNA and protein levels were markedly lower in EOC tissues compared with normal tissues. Silencing <i>SLFN11</i> enhanced EOC cell proliferation, migration, and invasion, whereas OE inhibited these malignant behaviors. <i>SLFN11</i> knockdown reduced PARPi-induced apoptosis and drug sensitivity, while its OE amplified these responses. Mechanistically, we demonstrate that <i>SLFN11</i> suppresses global proteotoxic ubiquitination, thereby specifically stabilizing PARP1/2 proteins and potentiating PARPi-mediated DNA damage through enhanced chromatin trapping. <i>SLFN11</i> enhances PARPi sensitivity in EOC by stabilizing PARP1/2 via inhibition of proteotoxic ubiquitination, supporting its role as a biomarker in a <i>BRCA</i>-wild-type EOC cell model where PARPi efficacy is limited by intrinsic resistance. While the application of PARPi in other subtypes of EOC still requires further validation, <i>SLFN11</i> may improve PARPi response and could be explored as a strategy to address PARPi resistance.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"226-240"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147461286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Estrogen, Dopamine, and Learning.","authors":"Carla E M Golden, Christine M Constantinople","doi":"10.1177/10445498261427138","DOIUrl":"10.1177/10445498261427138","url":null,"abstract":"<p><p>Estrogenic hormones act throughout the brain, yet the basic mechanisms by which hormones influence neural circuit dynamics and computations, especially during complex behaviors, are unclear. Exogenous estrogenic hormones modulate dopamine signaling in the nucleus accumbens, which is thought to promote synaptic plasticity for reward-based learning. We recently found that elevated estrogenic activity predicts enhanced phasic dopamine and behavioral sensitivity to past rewards that could be explained by reduced expression of dopamine reuptake proteins in the nucleus accumbens core. Our computational and decision theoretical approach allowed us to characterize estrogenic modulation of dopamine at broad levels of description and opens up new avenues of research on hormone-neuromodulatory interactions during cognitive behaviors.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"187-190"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147391963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silent Signals: The Expanding Role of Cell-Free DNA in Women's Health, Pregnancy, and Reproductive Medicine.","authors":"Matin Dolatabadi, Mahdieh Mondanizadeh","doi":"10.1177/10445498261426174","DOIUrl":"10.1177/10445498261426174","url":null,"abstract":"<p><p>Cell-free DNA (cfDNA) is an emerging biomarker detectable in various bodily fluids, with promising implications across a wide range of clinical domains. Its minimally invasive nature, short half-life, and ability to reflect tissue-specific genetic and epigenetic alterations position cfDNA as a key tool in women's health diagnostics. This narrative review aims to explore the biological characteristics, release mechanisms, and clinical utility of cfDNA in gynecological cancers, pregnancy-related disorders, and assisted reproductive technologies (ART), highlighting current applications, benefits, limitations, and future perspectives. A comprehensive literature review was conducted using databases including PubMed, Scopus, Web of Science, and Google Scholar. Relevant peer-reviewed articles from January 2005 to March 2025 were analyzed to summarize advances in cfDNA detection techniques, clinical applications, and emerging technologies in women's health. In gynecology, cfDNA-especially circulating tumor DNA-has shown promise in early cancer detection, mutation analysis, and disease monitoring. In prenatal medicine, fetal cfDNA (cffDNA) in maternal plasma enables highly accurate, noninvasive screening for chromosomal abnormalities and pregnancy complications such as preeclampsia and intrauterine growth restriction. In reproductive medicine, cfDNA derived from follicular fluid and embryo culture media may serve as a novel biomarker for assessing oocyte and embryo quality. cffDNA offers a noninvasive method for fetal genetic evaluation in pregnancy loss cases, enabling the detection of chromosomal abnormalities to inform clinical management. Technological innovations such as fragmentomics, methylation analysis, and artificial intelligence are enhancing the analytical power and clinical relevance of cfDNA. cfDNA offers a transformative, noninvasive approach for improving diagnosis, prognosis, and personalized care in women's health. While clinical implementation still faces technical and standardization challenges, emerging tools and multi-omics integration are expected to strengthen the role of cfDNA in precision medicine. Future large-scale studies and validation across diverse populations are essential to support its routine clinical adoption.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"201-213"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147438546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary Saturated Fatty Acids as Evolutionarily Conserved Signals of Immune Activation.","authors":"Sam J McCright, Olivia Harding, David A Hill","doi":"10.1177/10445498261427141","DOIUrl":"10.1177/10445498261427141","url":null,"abstract":"<p><p>Dietary fat is comprised largely of fatty acids (FAs), which function not only as metabolic substrates but also as key intracellular signaling molecules. Saturated fatty acids (SFAs) have long been linked to metabolic and inflammatory disease, yet the mechanisms by which they regulate immune function remain incompletely defined. In this review, we synthesize evidence that dietary SFAs directly modulate innate and adaptive immune responses through conserved inflammatory pathways. We highlight mechanisms of myeloid cell activation, including endoplasmic reticulum stress, inflammasome engagement, and NF-κB-dependent cytokine production, and discuss findings implicating SFAs in T cell activation and differentiation. We integrate recent work from our group demonstrating that dietary SFAs promote lung innate immune activation, linking lipid exposure to neutrophilic inflammation and impaired pulmonary function. Finally, we propose an evolutionary framework in which SFA-induced immune activation was adaptive during intermittent exposure but becomes maladaptive with chronic consumption, such as in modern diets.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"191-200"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147392001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compensatory Gene Regulation Following Survivin Inhibition in MDA-MB-231 Cells.","authors":"Manuel Antonio Martínez-Sifuentes, Juan Ramos-Treviño, Magali Espinosa-Castilla, Sheila Adela Villa-Cedillo, Iliana Encino-Ortega, Michelle Alejandra Muñoz-Dominguez, Pablo Ruiz-Flores, José Anselmo Hernández-Ibarra","doi":"10.1177/10445498261421790","DOIUrl":"10.1177/10445498261421790","url":null,"abstract":"<p><p>Breast cancer is the most diagnosed cancer in women and the second leading cause of cancer-related mortality worldwide. Advances in genetic technology have highlighted the heterogeneity of breast cancer, composed of various biological subtypes, with genetic profiling playing a crucial role in predicting chemotherapy response. This underscores the importance of identifying sensitive diagnostic and prognostic markers for early detection and developing more efficient targeted therapies. Among these, survivin, a protein linked to apoptosis inhibition and cell cycle regulation, is strongly expressed in various cancers, including breast cancer, where its overexpression is associated with poor prognosis and reduced survival rates. To analyze the effects of survivin gene inhibition in a triple-negative breast cancer (TNBC) model. The MDA-MB-231 cell line was stably transfected with short hairpin RNA targeting survivin, and the inhibition was validated via RT-qPCR and Western blot. Morphological evaluation, proliferation and migration assays, and a differential gene expression analysis using the GeneChip™ Human Gene 2.0 ST Array were performed. Statistical analyses were conducted with GraphPad Prism version 8 and Transcriptome Analysis Console. Survivin-inhibited MDA-MB-231-KD cells exhibited evident morphological changes, reduced migration capacity, and altered expression of genes such as <i>BCL2, COX1, COX2, VGF, BIR2</i>, and <i>CDC20</i>, involved in key cancer signaling pathways. Inhibition of survivin in this TNBC model induces critical cellular changes and significantly alters gene expression associated with tumor progression, highlighting its potential as a therapeutic target.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"214-225"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147438576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating Network Pharmacology, Transcriptome Analysis, and In Vitro Experiment to Investigate Molecular Mechanism of Liensinine on Pancreatic Cancer.","authors":"Jiawei Cao, Jiaqi Yao, Shoudi He, Yifeng Wu","doi":"10.1177/10445498261428954","DOIUrl":"10.1177/10445498261428954","url":null,"abstract":"<p><p>Liensinine (LIE), a bioactive alkaloid from Nelumbo nucifera, exhibits proapoptotic and anticancer properties. Its effect and mechanism in pancreatic cancer remain unexplored, representing a novel research direction. We employed an integrated strategy combining network pharmacology, transcriptome sequencing, and experimental validation to investigate LIE's action against PANC-1 pancreatic cancer cells. Key targets and pathways were identified via bioinformatics analyses. Molecular docking and survival analysis were conducted to verify core targets. In vitro assays including CCK-8, lactate dehydrogenase release, Hoechst/PI staining, flow cytometry, wound healing, and transwell invasion were used to assess cytotoxicity, apoptosis, migration, and invasion. Western blotting validated protein-level changes. Network pharmacology revealed 90 overlapping targets of LIE and pancreatic cancer, with the Phosphatidylinositol 3-k (PI3K)/Serine/Threonine Kinase (AKT) pathway being significantly enriched. Molecular docking indicated a strong binding affinity of LIE to Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Alpha (PIK3CA) and AKT1. Survival analysis associated high PIK3CA expression with poorer prognosis in pancreatic cancer patients. In vitro, LIE dose-dependently inhibited PANC-1 cell proliferation, migration, and invasion while significantly inducing apoptosis. Western blotting confirmed that LIE treatment effectively suppressed the activation of the PI3K/AKT signaling pathway. Our study is the first to demonstrate that LIE exerts potent antitumor effects against pancreatic cancer cells by inducing apoptosis and inhibiting malignant phenotypes through suppression of the PI3K/AKT pathway. These findings highlight LIE as a promising novel therapeutic candidate for pancreatic cancer treatment.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"241-251"},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLC25A30 Regulates Mitochondrial Autophagy Through the PINK1/PARKIN Signaling Pathway to Alleviate Sepsis-Associated Acute Kidney Injury.","authors":"Mingyu Xu, Yuchen Wang, Wuyang Lv, Yingyue Ding, Jing Liu, Ruxue Diao, Xiaotong Ma, Mengjiao Yin, Yingyu Jin","doi":"10.1177/10445498261442835","DOIUrl":"https://doi.org/10.1177/10445498261442835","url":null,"abstract":"<p><p>This study aims to investigate the expression of the SLC25 subfamily in sepsis-associated acute kidney injury (SA-AKI) and the role of <i>SLC25A30</i> in regulating PINK1/PARKIN-mediated mitophagy. Transcriptome sequencing of renal tissues from lipopolysaccharide (LPS)-induced SA-AKI rats at multiple time points revealed time-dependent differential expression of SLC25 genes. At 12 h post-LPS injection (renal injury peak), 11 differentially expressed genes were identified. Intersection with Gene Expression Omnibus datasets and Gene Ontology enrichment highlighted 11 codifferentially expressed genes enriched in mitochondrial transmembrane transport. Notably, <i>SLC25A30</i> was significantly negatively correlated with KIM-1 (<i>r</i> = -0.96) and LCN2 (<i>r</i> = -0.98). <i>SLC25A30</i> was significantly downregulated in SA-AKI rat renal tissues and LPS-induced HK-2 cells, accompanied by upregulated PINK1/PARKIN, excessive mitophagy (elevated LC3B-II, decreased p62), and increased renal injury markers. <i>SLC25A30</i> overexpression inhibited PINK1/PARKIN, reversed excessive mitophagy, reduced KIM-1 and LCN2 levels, alleviated mitochondrial dysfunction, enhanced cell viability, and exerted cytoprotective effects. <i>PINK1</i> knockdown attenuated the regulatory effect of <i>SLC25A30</i> on excessive mitophagy, indicating a dependence on the PINK1/PARKIN pathway. In conclusion, downregulated <i>SLC25A30</i> is closely associated with excessive mitophagy in SA-AKI. <i>SLC25A30</i> overexpression inhibits excessive mitophagy via downregulating the PINK1/PARKIN pathway, improves mitochondrial function, and alleviates HK-2 cell injury, suggesting that <i>SLC25A30</i> may be a novel molecular target for SA-AKI-targeted therapy.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"10445498261442835"},"PeriodicalIF":2.6,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147792939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intervention Study on the Regulation of circAno6/miR-296-3p/TLR4 Signaling Axis by Shugan Jianpi Formula to Alleviate Inflammation Cascade and Inhibit HSC Activation.","authors":"Qian Wu, Tingting Li, Jing Qu, Chang Fan, Lili Zhang, Hui Jiang","doi":"10.1177/10445498261442830","DOIUrl":"https://doi.org/10.1177/10445498261442830","url":null,"abstract":"<p><p>Liver fibrosis (LF) is a fibrotic and inflammatory condition resulting from chronic liver damage, and the activation of hepatic stellate cells (HSCs) is the central event. Our prior research has revealed that the circAno6/miR-296-3p/Toll-like receptor (TLR4) pathway is a key signaling axis in the pathogenesis of LF. Shugan Jianpi Formula (SGJPF) is a traditional Chinese medicinal treatment widely used to treat LF. We hypothesized that SGJPF exerts anti-LF effects by modulating the circAno6/miR-296-3p/TLR4 signaling axis, attenuating inflammatory responses, and inhibiting HSC activation, thereby ultimately mitigating LF. In this study, an SGJPF extraction solution was first prepared and administered to rats via gavage at a specified dosage. Blood samples were subsequently collected from the abdominal aorta to prepare SGJPF-containing serum. Optimal SGJPF intervention conditions were determined using the Cell Counting Kit-8 assay. Flow cytometry was used to assess JS-1 cell cycle progression. The levels of interleukin-1 beta (IL-1β) and IL-18 were measured by enzyme-linked immunosorbent assay. The expression levels of collagen type I (collagen I), α-smooth muscle actin (α-SMA), circAno6, TLR4, miR-296-3p, and NOD-like receptor protein 3 (NLRP3) were evaluated using Western blotting, immunofluorescence, and real-time quantitative polymerase chain reaction. The results indicated that the optimal intervention condition involved serum containing 20% SGJPF, which was administered for a duration of 48 h. SGJPF-containing serum has been shown to reduce the viability of JS-1 cells and decrease the cell count in the G2 + S phase, thereby affecting HSC function. Furthermore, SGJPF-containing serum effectively suppressed the expression levels of NLRP3, IL-1β, IL-18, collagen I, α-SMA, circAno6, and TLR4 while upregulating miR-296-3p expression. These findings suggest that SGJPF can modulate the activity of the circAno6/miR-296-3p/TLR4 signaling axis, attenuate inflammatory responses, and inhibit HSC activation, thereby mitigating LF.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"10445498261442830"},"PeriodicalIF":2.6,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}