Biocell最新文献

{"title":"C-Myc Reduces Oxygen-Glucose Deprivation/Reperfusion-Induced Neuronal Pyroptosis through the SRSF1/NLRP1 Axis","authors":"Siliang Liu, Hong Tang, Ying Xia, Zhengtao Yu, Ning Gao","doi":"10.32604/biocell.2025.064396","DOIUrl":"https://doi.org/10.32604/biocell.2025.064396","url":null,"abstract":"Objectives: NOD-like receptor family pyrin domain-containing (NLRP) 1-mediated pyroptosis plays a key role in the pathogenesis of cerebral ischemia-reperfusion injury (CIRI). C-Myc is reported to play a major role in CIRI. However, the mechanism remains unclear. This study aimed to investigate whether c-Myc affects CIRI by regulating Serine/Arginine-rich Splicing Factor 1 (SRSF1)/NLRP1-mediated pyroptosis. Methods: Oxygen-glucose deprivation/reperfusion (OGD/R) induced neuroblastoma cells for the establishment of an in vitro CIRI model. The levels of c-Myc and SRSF1, cell viability, the expression of pyroptosis-related factors, and the interaction between SRSF1 and NLRP1 were evaluated. Results: The expression of c-Myc and SRSF1 was decreased in OGD/R-induced neuroblastoma cells. c-Myc overexpression increased c-Myc and SRSF1 expression and cell viability in OGD/R-induced neuroblastoma cells while inhibiting NLRP1, Caspase1, apoptosis-associated speck-like protein containing a CARD (ASC), interleukin-1beta (IL-1β), IL-18, and lactate dehydrogenase levels and pyroptosis. C-Myc was positively correlated with SRSF1. SRSF1 low expression reversed the effects of c-Myc on the above indicators in OGD/R-induced neuroblastoma cells. Mechanically, SRSF1 interacted with NLRP1. SRSF1 was negatively correlated with NLRP1. The NLRP1 activator muramyl dipeptide (MDP) reversed the SRSF1 effect on OGD/R-induced neuroblastoma cells. Conclusion: Our results indicated that c-Myc reduced OGD/R-induced neuroblastoma cell pyroptosis by inhibiting NLRP1 activation by positive feedback SRSF1 signal. Our findings suggested that the c-Myc/SRSF1 axis might be a new strategy for treating CIRI in the clinic.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 7","pages":"1245-1264"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147888579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive Analysis of the Expression Levels and Prognostic Values of SENP Family Genes in Liver Hepatocellular Carcinoma","authors":"Shang Kong, Danting Li, Huyan Meng, Haoxiang Zhang, Xiaochun Jiang, Peilin Zheng, Shoujun Huang","doi":"10.32604/biocell.2025.066205","DOIUrl":"https://doi.org/10.32604/biocell.2025.066205","url":null,"abstract":"Background: Small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) cleave the isopeptidic bond between SUMO1/2/3 and protein substrates, thus regulating the structure, activity, and lifetime of a variety of proteins... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 8","pages":"1481-1504"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147914262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N-Acetyl Cysteine Inhibits Weaning Stress-Induced Intestinal Cell Cycle Arrest in Piglets through Decreasing ERK, JNK, and p38 Phosphorylation","authors":"Qi Guo, Jianxiong Xu, Xuan Cai, Jiaojiao Xie, Siqi Wu","doi":"10.32604/biocell.2025.063568","DOIUrl":"https://doi.org/10.32604/biocell.2025.063568","url":null,"abstract":"Objectives: Weaning induces oxidative stress in pigs, increasing the risk of diarrhea and death. Intestinal damage is associated with obstructed intestinal cell cycles. To stop damage caused by reactive oxygen species (ROS), N-acetyl cysteine (NAC) has been widely employed. In this study, we examined changes in the intestinal cyclin of weaning piglets and assessed the impact of NAC on intestinal cell cycle arrest and intracellular signaling pathways. Methods: We conducted two animal experiments. In the first, we divided 12 litters of 120 newborn piglets into two groups: a control group and a weaning group. The control piglets were allowed to suckle normally. The weaning group was weaned after 3 weeks and fed a normal diet for piglets. We slaughtered six piglets from the control group and six from the weaning group. We observed cyclin changes and intestinal development at days 0, 1, 4, and 7 after weaning. In the second experiment, we divided 15 litters of 150 piglets that were 2 weeks old into three groups: the control group, the weaning group, and the NAC group. Control piglets were allowed to suckle normally. Piglets in the weaning and NAC groups were weaned when they were 21 days old. The NAC group was fed a basal diet supplemented with 500 mg/kg NAC, and the weaning group was fed the basal diet alone. The experimental period was 14–25 days of age. Four days after weaning, we slaughtered one piglet from each litter. We then analyzed intestinal cell cycle indexes, intestinal oxidative stress, c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 phosphorylation. Results: Weaning decreased the piglets’ feed intake and daily gain, reduced the serum antioxidant capacity, and increased the intestinal ROS level. Furthermore, the jejunum histology and barrier development of the jejunum exhibited damage after weaning, the microvilli displayed hypoplasia, and the p21 and p27 protein expression levels of the jejunum were significantly elevated. We did not observe any significant differences in cyclin D and E after days 1, 4, and 7 post-weaning compared with the control group. We observed, however, significantly increased cyclin D and E expression, lower ERK, JNK, and p38 kinase phosphorylation; villus atrophy alleviation; decreased p21 and p27 expression; and increased average daily intake of feed and weight gain. Conclusion: This research demonstrates that weaning stress inhibits piglet intestinal proliferation by reducing cyclin D and cyclin E expression. NAC downregulates p21 and p27 through modulating mitogen-activated protein kinases (MAPKase) phosphorylation, thereby promoting cell proliferation. The results indicate that NAC promotes intestinal function and the integrity of enterocytes and holds promise as a new feed additive for animal health.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 5","pages":"907-924"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147899930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ANLN Promotes Cervical Cancer Cell Proliferation, Migration and Invasion and Suppresses Apoptosis via the Wnt/β-Catenin Pathway","authors":"Lingling Zhang, Jianping Xiong, Yawen Liu, Lei Li, Hualing Wang","doi":"10.32604/biocell.2025.061585","DOIUrl":"https://doi.org/10.32604/biocell.2025.061585","url":null,"abstract":"Objective: Anillin (ANLN) is considered an oncogene in various cancers, but its effect on cervical cancer remains poorly understood. Hence, this study aimed to describe the action of ANLN on cervical cancer development and i... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 2","pages":"253-267"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147884724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring Neutrophil Extracellular Traps in Cardiovascular Pathologies: The Impact of Lipid Profiles, PAD4, and Radiation.","authors":"Siarhei A Dabravolski, Michael I Bukrinsky, Aleksandra S Utkina, Alessio L Ravani, Vasily N Sukhorukov, Alexander N Orekhov","doi":"10.32604/biocell.2025.062789","DOIUrl":"10.32604/biocell.2025.062789","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NET) have emerged as critical players in the pathogenesis of atherosclerosis and other cardiovascular diseases (CVD). These web-like structures, composed of DNA, histones, and granule proteins released by neutrophils, contribute significantly to both inflammation and thrombosis. This manuscript offers a comprehensive review of the recent literature on the involvement of NET in atherosclerosis, highlighting their interactions with various pathophysiological processes and their potential as biomarkers for CVD. Notably, the impact of radiation on NET formation is explored, emphasising how oxidative stress and inflammatory responses drive NET release, contributing to plaque instability. The role of histones, particularly citrullinated histones, in endothelial dysfunction and plaque progression is discussed, highlighting their significance in the pathophysiology of atherosclerosis. Furthermore, the complex relationship between lipoproteins and NET formation is examined, with a focus on how elevated low-density lipoprotein (LDL) and decreased high-density lipoprotein (HDL) levels facilitate NET release, thus promoting vascular inflammation and plaque instability. The influence of cholesterol on NET formation is also explored, underscoring its contribution to plaque development and stability. The role of Peptidylarginine deiminase 4 (PAD4) in the regulation of NETosis is reviewed, with attention given to how PAD4-driven citrullination of histones affects atherosclerosis progression. Moreover, the manuscript examines the potential of NET components-such as double-stranded DNA, myeloperoxidase-DNA complexes, and citrullinated histone H3-as biomarkers for assessing disease severity and predicting adverse cardiovascular events, including ST-elevation myocardial infarction (STEMI) and stroke. Elevated levels of these biomarkers correlate with worse clinical outcomes, suggesting their utility in guiding therapeutic interventions. In contrast to the existing body of work, this review highlights the novelty of integrating recent findings on NET interactions with lipid metabolism, histone modifications, and PAD4 activity in the context of atherosclerosis. Overall, NET plays an integral role in the inflammatory and thrombotic processes underpinning atherosclerosis, and their components hold promise as both diagnostic markers and therapeutic targets in cardiovascular disease management.</p>","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 6","pages":"931-959"},"PeriodicalIF":1.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12333638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144818362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA CRYBG3 Regulates Adaptive Radioresistance in Non-Small Cell Lung Cancer Cells through the p53/HSF1/TRAP1 Axis","authors":"Xiangyu Yan, Yusheng Jin, Yan Yuan, Xubaihe Zhang, Jun Li, Ying Xu, Yangyang Ge, Anqing Wu","doi":"10.32604/biocell.2025.066935","DOIUrl":"https://doi.org/10.32604/biocell.2025.066935","url":null,"abstract":"Objectives: Fractionated radiotherapy represents a standardized and widely adopted treatment modality for cancer management, with approximately 40% of non-small cell lung cancer (NSCLC) patients receiving it. However, repeated irradiation may induce radioresistance in cancer cells, reducing treatment effectiveness and raising recurrence risk. The long noncoding RNA CRYBG3 (lncRNA CRYBG3), which is upregulated in lung cancer cells after X-ray irradiation, contributes to the radioresistance of NSCLC cells by promoting wild-type p53 protein degradation. This study aims to elucidate the mechanism of fractionated irradiation-induced radioresistance, in which lncRNA CRYBG3 regulates radiation-induced mitochondrial damage and reactive oxygen species (ROS) generation through the p53 downstream signaling pathway. Methods: To investigate the critical roles of lncRNA CRYBG3 in mediating radioresistance induced by fractionated irradiation in NSCLC, we established radioresistant NSCLC cells by irradiating the A549 and H460 cell lines with 60 Gy of X-rays in 12 fractions, and named the radioresistant cells A549R and H460R, respectively. Lentiviral vectors were used to deliver short hairpin RNA (shRNA) into cells to knock down lncRNA CRYBG3, thereby investigating its contribution to adaptive radioresistance in A549R and H460R cells. All cells were irradiated with 4 Gy of X-rays, and subsequent analyses were conducted to evaluate mitochondrial damage, ROS generation, apoptosis, and the expression of oxidative stress-related proteins. Results: Increased expression levels of lncRNA CRYBG3 were positively associated with the acquisition of radioresistance in NSCLC cells. Additionally, suppressing lncRNA CRYBG3 increased mitochondrial damage and promoted radiation-induced apoptosis in radioresistant NSCLC cells. Mechanistically, the downregulation of lncRNA CRYBG3 led to increased p53 levels, resulting in decreased expression of heat shock factor 1 (HSF1) and tumor necrosis factor receptor-associated protein 1 (TRAP1), as well as enhanced radiation-induced mitochondrial oxidative damage and apoptosis. Conclusion: The results indicate that lncRNA CRYBG3 plays a regulatory role in adaptive radioresistance in NSCLC cells through the p53/HSF1/TRAP1 axis. Therefore, targeting lncRNA CRYBG3 could potentially improve the efficacy of fractionated radiotherapy in NSCLC.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"0 0","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of Transcription Factor Krüppel-Like Factor 3 Expression in Splenic T Lymphocytes and Association with Immune Status in Septic Mice","authors":"Miao Yan, DONGXUAN CHI, Wen Wang, PEI PEI, Min Xie, SHUANGLING LI","doi":"10.32604/biocell.2025.063622","DOIUrl":"https://doi.org/10.32604/biocell.2025.063622","url":null,"abstract":"Background: Transcription factor Krüppel-like factor 3 (KLF3) may be involved in regulating inflammation and lymphocyte function. Immune dysfunction in sepsis involves both hyper-inflammation and immunosuppression. However, studies on T-lymphocyte KLF3 expression in sepsis are lacking. Methods: We induced sepsis in mice via cecal ligation and puncture (CLP), and their survival rate over 7 days was evaluated. To identify the immune status of these mice, we assessed their cytokine levels, organ damage scores, and splenic T-lymphocyte phenotype. Finally, T-lymphocyte KLF3 expression was detected through flow cytometry. Results: Over the 7 days of observation, septic mice demonstrated 64.7% mortality. In the early stages after CLP, the proinflammatory and anti-inflammatory cytokine levels increased rapidly, multiple organ damage occurred, and splenic T lymphocytes became activated. However, the proportion of KLF3+ T lymphocytes decreased. Subsequently, cytokine levels and lymphocyte activation decreased. An increase in cell apoptosis led to a substantial loss of T lymphocytes. Combined with the continual elevations in serum interleukin levels and worsening severe organ damage, septic mice may have entered a state of persistent inflammation and immunosuppression, with a simultaneous increase in KLF3 expression in T lymphocytes. Notably, KLF3 expression was negatively correlated with T-lymphocyte activation and apoptosis. Conclusions: In our septic mice, splenic T-lymphocyte KLF3 expression decreased in the early stage when the mice exhibited a systemic inflammatory response and T-lymphocyte activation. In contrast, it increased in the later stage, when persistent inflammation and immunosuppression occurred. Dynamic monitoring of KLF3 expression levels may provide aid in identifying the immune status of sepsis.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 5","pages":"893-906"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147896007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of Dendritic Cell Function by RFX5 through Interaction with HDAC2 and Its Mechanism in Pediatric Asthma","authors":"Yahui Wu, Tiansheng Dai, Jingwen Qin, Jian Guo, Jitao Fan, Jun Mei, LI Xiao-li, Fang Liu","doi":"10.32604/biocell.2025.061289","DOIUrl":"https://doi.org/10.32604/biocell.2025.061289","url":null,"abstract":"Background: Dendritic cells (DCs) play a pivotal role in antigen presentation and regulating adaptive immune responses in asthma pathophysiology. However, the underlying molecular mechanisms remain incompletely understood. M... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 4","pages":"701-720"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147891235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of Liriodendrin on NLRP3-Mediated Pyroptosis and Proinflammatory Pathways in Mice Experiencing Acute Respiratory Distress Syndrome Induced by Lipopolysaccharide","authors":"Kuo‐Yang Huang","doi":"10.32604/biocell.2025.061073","DOIUrl":"https://doi.org/10.32604/biocell.2025.061073","url":null,"abstract":"Background: Acute respiratory distress syndrome (ARDS) is the major therapeutic dilemma associated with significant inflammation and severe pulmonary dysfunction. Liriodendrin is a bioactive compound extract from ... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 2","pages":"315-334"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147913824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CLDN9 Levels Influence the Biological Activities of Cells in Gastric Cancer","authors":"Jin Liu, Xiu Zhang, Xiao Hu, Gaofeng Yuan, Kai Chen","doi":"10.32604/biocell.2025.063296","DOIUrl":"https://doi.org/10.32604/biocell.2025.063296","url":null,"abstract":"Objective: This study examines the significance and functions of CLDN9 in gastric cancer (GC), intending to identify novel targets for diagnosis and treatment. Methods: CLDN9 expression in GC tissues and cell lines was inves... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 4","pages":"665-680"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147884858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}