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Chung-Che Tsai^1,#, Chih-Hung Lin^2,#, Katherine Lin^3,4, Jia Hong Hubert Chen^4,5, Ying Jie Celia Chen^4,5, Ilyssa Ting-Ying Chang^3,4, Hsu-Hung Chang⁶, Jin-Yin Chang⁷, Tin-Yi Chu⁸, Po-Chih Hsu^4,8,*, Chan-Yen Kuo^8,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2025.073698 - 23 March 2026
Abstract Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide, most commonly driven by chronic hepatitis B virus (HBV) infection. The HBV X protein (HBx) plays a central role in hepatocarcinogenesis by regulating transcription, signal transduction, epigenetic modification, and interactions with noncoding RNAs. This review summarizes current advances in HBx-mediated signaling pathways and mutation-specific functions, highlighting its potential as a prognostic biomarker and therapeutic target, and providing insights for future strategies in HCC treatment and HBV eradication. Activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), cAMP response element binding protein/activating transcription factor More >

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Congwei You^1,#, Anwen Yin^2,#, Jia Xia³, Le Zhang^4,*, Xiaolei Wang^1,*, Yutong Hou^4,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2025.072971 - 23 March 2026
Abstract Metabolic dysfunction-associated fatty liver disease (MAFLD) and chronic kidney disease (CKD) have shown a marked global increase in prevalence, placing a substantial burden on public health and healthcare systems worldwide. Epidemiological data demonstrate a significant overlap between these two conditions, with further evidence from research identifying common pathophysiological features, such as lipid metabolism dysregulation, disrupted energy balance, and chronic systemic inflammation. Mitochondria are central to the pathophysiology of both diseases. In addition to their role in energy production, mitochondria are involved in numerous critical cellular processes, including biosynthesis, lipid metabolism, oxidative phosphorylation, signal transduction, and More >

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675

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Joongbum Moon¹, Ji Hyeon Ahn², Moo-Ho Won^3,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2025.072635 - 23 March 2026
（This article belongs to the Special Issue: Cellular and Molecular Insights into Brain Ischemic Insults)
Abstract Ischemia-reperfusion (I/R) injury induces region-specific neuronal vulnerability within the hippocampus, with the cornu ammonis 1 (CA1) subfield particularly prone to delayed neuronal death. While intrinsic neuronal factors have been implicated, emerging evidence highlights the decisive contribution of astrocyte endfeet (AEF)—specialized perivascular structures that regulate ion and water homeostasis, glutamate clearance, and blood–brain barrier (BBB) stability. This review synthesizes structural and molecular alterations of AEF across the CA1–CA3 subfields following I/R and their correlation with neuronal fate. In CA1, AEF undergo early-onset swelling and detachment from the vascular basal lamina due to dysfunction of critical proteins… More >

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Kawaljit Kaur^*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2025.073340 - 23 March 2026
（This article belongs to the Special Issue: Novel Targeted Therapy in Oncology)
Abstract Diffuse intrinsic pontine glioma (DIPG) is a pediatric brainstem tumor with a very poor prognosis, characterized by immunosuppressive tumor microenvironment (TME) that limits immune infiltration, including a significant reduction in circulating natural killer (NK) cells. This drop in NK cell levels and activity may promote tumor growth and immune evasion, making NK cells a promising target for immunotherapy. NK cells can attack and eliminate DIPG tumor cells, including glioma stem cells, while counteracting certain immune evasion strategies. Although the DIPG microenvironment and blood-brain barrier present challenges, NK cell-based therapies have shown encouraging tumor control and… More >

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822

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Huan Zhou¹, Jiami Jiang², Yuqing Zou¹, Jiahui Zhang^1,*, Zhiwei Yu^3,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2025.073989 - 23 March 2026
Abstract Obesity-related asthma is a distinct clinical phenotype, characterized by severe respiratory symptoms, reduced responsiveness to conventional glucocorticoid therapy, and a significantly increase in disease burden. With the rising global prevalence of obesity, the number of individuals affected by obesity-related asthma is steadily growing, presenting a pressing public health issue. The pathogenesis of obesity-related asthma is multifactorial, involving a complex interplay of metabolic and immune pathways. Key mechanisms include dysregulated T-cell differentiation, pro-inflammatory macrophage polarization, oxidative stress, and altered cytokines and adipokines secretion, all contributing to airway inflammation and remodeling. Additionally, metabolic factors, such as adiposity… More >

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548

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Alessio L. Ravani¹, Michael I. Bukrinsky², Anastasia V. Poznyak^3,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2025.074266 - 23 March 2026
（This article belongs to the Special Issue: Molecular Basis for the Involvement of Inflammation and Lipids in Pathologies)
Abstract Atherosclerosis (AS) remains a major contributor to cardiovascular disease (CVD) mortality worldwide. Its development involves dysregulated lipid handling, persistent vascular inflammation, and endothelial cell (EC) dysfunction, influenced by genetic, environmental, and lifestyle factors. Increasing evidence highlights a pivotal role of endoplasmic reticulum (ER) stress as a molecular link between lipid dysregulation and inflammatory signaling in AS pathogenesis. ER stress is triggered by modified LDL, oxidized lipids, hyperhomocysteinemia, oxidative stress (OS), and disrupted calcium (Ca²⁺) homeostasis, leading to activation of the unfolded protein response (UPR). Core UPR mediators—inositol-requiring enzyme 1 (IRE1), protein kinase RNA-like ER kinase (PERK),… More >

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1348

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633

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Jingfei Shi^#, Yi Ding^#, Hui Lu^*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.073956 - 23 March 2026
（This article belongs to the Special Issue: Autoantibodies and Emerging Biomarkers in Immune-Mediated Neurological Disorders)
Abstract Objective: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Soluble interleukin-2 receptor alpha (sIL-2Rα) has been implicated in MS pathogenesis, but its mechanisms remain unclear. This study investigates how sIL-2Rα exacerbates MS by modulating microglial activation and antibody-dependent cellular cytotoxicity (ADCC) in an experimental autoimmune encephalomyelitis (EAE) mouse model. Methods: Female C57BL/6J mice were induced with EAE and treated with sIL-2Rα. Clinical symptoms, histopathology, and molecular changes were analyzed. Microglial activation was assessed via immunohistochemistry, Western blot, and RNA sequencing. In vitro, ADCC-mediated oligodendrocyte injury was evaluated using More >

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249

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Abdullah Alattar¹, Reem Alshaman¹, Fawaz E. Alanazi¹, Yusuf S. Althobaiti², Ghareb M. Soliman³, Waleed Salman Khubrni¹, Howaida S. Ali⁴, Fawad Ali Shah^5,6,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.074865 - 23 March 2026
（This article belongs to the Special Issue: Neuroinflammation and Neuroprotection in CNS Diseases: From Mechanisms to Therapeutic Targets)
Abstract Objectives: Permanent middle cerebral artery occlusion (pMCAO) can lead to hippocampal damage through multiple linked pathways such as reactive oxidative stress (ROS), neuroinflammation mediated by NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), tumour necrosis factor-alpha (TNF-α), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and glutamate excitotoxicity involving N-methyl-D-aspartate receptor subunits 2a and 2b (NR2a/NR2b) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR/GluR1). The hippocampus, which is essential for memory and cognition, is at a substantial risk of ischemic degeneration. The aim of this study was to investigate the neuroprotective potential of melatonin in regulating these… More >

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256

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Gerardo Ramírez-Mejía^1,#, Sofía Plata-Burgos^1,#, Raquel Cuevas-Díaz Duran², Adrian Ledesma-Beiza¹, Cynthia Sámano¹, Thalía Estefanía Sánchez-Correa³, Ernesto Soto-Reyes^1,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.075061 - 23 March 2026
（This article belongs to the Special Issue: Cellular Mechanisms in Neurodegeneration, Injury, and Regeneration)
Abstract Objectives: Glioblastoma multiforme (GBM) is a highly aggressive brain tumor characterized by extensive transcriptional and epigenetic dysregulation. Brother of the Regulator of Imprinted Sites (BORIS/CTCFL) has been implicated in oncogenic transcriptional programs in several cancers, but its role in GBM remains poorly defined. This study aimed to characterize BORIS-associated transcriptional programs in GBM and to assess their functional relevance using integrative computational and experimental approaches. Methods: Transcriptomic data from The Cancer Genome Atlas (TCGA)-GBM and Genotype-Tissue Expression (GTex) brain cortex were analyzed following batch correction, differential expression analysis, and gene ontology enrichment. TCGA-GBM samples were… More >

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241

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Kai Tang¹, Shengxing Lu¹, Cuie He², Ruozeng Rong^1,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.072154 - 23 March 2026
Abstract Objectives: Prostate cancer (PCa) is a highly prevalent male malignancy with limited efficacy in advanced stages. Dysregulated modulation of necroptosis was reported to be tightly correlated with PCa initiation and progression. Herein, we aimed to identify necroptosis-associated long non-coding RNAs (lncRNAs) and delineate their functional roles in PCa through an integrated approach combining bioinformatic analyses and in vitro experimental validation. Methods: RNA sequencing data and corresponding clinical information of PCa were downloaded from The Cancer Genome Atlas (TCGA). Differentially expressed necroptosis-related genes (NRGs) and lncRNAs were screened, and necroptosis activity was assessed by single-sample gene set… More >

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562

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255

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Yuanhong Mao^#, Yunlan Yang^#, Kun Yang^§, Yongqiang Sun, Kun Yang^*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.075138 - 23 March 2026
Abstract Objective: Intestinal barrier disruption is a critical event in sepsis and ischemia–reperfusion (I/R) injury. Enteric glial cells (EGCs) maintain barrier integrity by secreting glial cell line–derived neurotrophic factor (GDNF). This study aimed to determine whether Dexmedetomidine (Dex) protects the intestinal barrier via α7-nicotinic acetylcholine receptor (α7-nAChR) signaling in EGCs. Methods: An in vitro EGC-intestinal epithelial cell (IEC) co-culture system and a murine intestinal I/R model were established. EGCs were selectively ablated in vivo using benzalkonium chloride (BAC). Barrier integrity was evaluated by transmembrane electrical resistance (TEER) and plasma FITC-dextran permeability. Enzyme-Linked Immunosorbent Assay (ELISA) and Western blotting… More >

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221

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Semin Lee^1,2,#, Minjun Kim^3,4,#, Seungmin Lee^2,5, Jiyun Yoo^1,5, Soo Seok Hwang^6,7, Seongchan Kim⁸, Seung Pil Yun^9,10, Dong Kyu Choi^11,12,*, Sangdun Choi^13,14,*, Hyuk-Kwon Kwon^1,2,5,*
BIOCELL, Vol.50, No.3, 2026, DOI:10.32604/biocell.2026.074555 - 23 March 2026
Abstract Objective: Cisplatin is a widely used chemotherapeutic agent due to its ability to damage DNA in the treatment of cancer. However, its clinical application is often limited by adverse effects on normal tissues, especially the kidneys. Understanding the molecular mechanisms of cisplatin-induced nephrotoxicity is crucial for developing strategies to mitigate its side effects. In this study, we aimed to elucidate the molecular mechanisms underlying cisplatin-induced DNA damage and apoptosis in human renal epithelial cells, with a focus on key signaling pathways and mediators that drive nephrotoxicity. Methods: To explore these mechanisms, human proximal tubule epithelial… More >

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