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  • Open Access

    REVIEW

    Emerging Role of ACOD1/Itaconate in Cancer: Bridging Metabolic Reprogramming and Signaling in the Tumor Microenvironment

    Xing-Guo Li1,2,3,#, Lu-Kai Wang4,#, Fu-Ming Tsai5, Hsueh-Chun Wang1,*

    BIOCELL, DOI:10.32604/biocell.2026.075492

    Abstract Itaconate, produced by aconitate decarboxylase 1 (ACOD1, also known as IRG1), acts as a key immunometabolite that inhibits succinate dehydrogenase (SDH) and can engage reduction-oxidation (redox)-sensitive signaling programs. This review summarizes the emerging, context-dependent roles of the ACOD1-itaconate axis in cancer, while critically distinguishing between the effects of endogenous itaconate and its cell-permeable derivatives. In tumor cells, endogenous ACOD1 expression or uptake via solute carrier family 13 member 3 (SLC13A3) alters oxidative phosphorylation and glycolysis. In the tumor microenvironment, myeloid-derived itaconate contributes to immune tolerance by reducing dendritic-cell cross-priming and limiting CD8+ T-cell metabolic activity. Moreover, More >

  • Open Access

    Flow Cytometry Study of Immune Cell Subpopulations from the Mouse Vertebral Bone Marrow and Intervertebral Disc Following Endplate Microfracture

    Dalin Wang1, Mingcai Zhang1, Richard Hastings2, Patrick George1, Ryan Ranzau1, Jinxi Wang1,3,*

    BIOCELL, DOI:10.32604/biocell.2026.074572

    Abstract Objective: Although endplate (EP) injury may cause intervertebral disc (IVD) degeneration and Modic changes (MCs) in the vertebral bone marrow (VBM), EP injury-induced synchronous cellular reactions and their crosstalk in the IVD and VBM remain unclear. This protocol-based study aimed to streamline and optimize the methods of tissue harvest and cell preparation for flow cytometry (FCM) analysis of T-cell and macrophage subpopulations in both VBM and IVD adjacent to the surgically induced EP microfracture in mice. Methods: EP injury or sham procedure was performed at the spinal levels L4-5 and L5-6 in male mice. Step-by-step… More >

  • Open Access

    ARTICLE

    ERK- and p53-Mediated ATF3 Expression Contributes to Cisplatin-Induced DNA Damage in Renal Epithelial Cells

    Semin Lee1,2,#, Minjun Kim3,4,#, Seungmin Lee2,5, Jiyun Yoo1,5, Soo Seok Hwang6,7, Seongchan Kim8, Seung Pil Yun9,10, Dong Kyu Choi11,12,*, Sangdun Choi13,14,*, Hyuk-Kwon Kwon1,2,5,*

    BIOCELL, DOI:10.32604/biocell.2026.074555

    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 >

  • Open Access

    ARTICLE

    KDM6B Regulates the Tumor Microenvironment and Promotes EMT via the PI3K/AKT/mTOR Signaling in Differentiated Thyroid Cancer

    Jiangtao Yu*, Qingfeng Huo, Xinxin Duan

    BIOCELL, DOI:10.32604/biocell.2026.073331

    Abstract Objectives: The tumor microenvironment and epithelial-mesenchymal transition (EMT) are closely linked to the progression of differentiated thyroid cancer (DTC). However, the functional mechanisms of lysine-specific demethylase 6B (KDM6B) in carcinogenesis remain incompletely understood. This study aims to clarify whether KDM6B affects DTC progression and EMT through the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of the rapamycin (PI3K/AKT/mTOR) pathway, providing a potential target for clinical treatment of DTC. Methods: Tissue samples from DTC patients (n = 39) were collected, and KDM6B expression was determined through Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blot. Cell counting kit-8 assay, 5-Ethynyl-2-deoxyuridine… More > Graphic Abstract

    KDM6B Regulates the Tumor Microenvironment and Promotes EMT via the PI3K/AKT/mTOR Signaling in Differentiated Thyroid Cancer

  • Open Access

    ARTICLE

    BORIS/CTCFL Reprograms Glioblastoma Transcriptional Networks through the Regulation of Tumor-Associated Genes such as CD36 and FBN2

    Gerardo Ramírez-Mejía1,#, Sofía Plata-Burgos1,#, Raquel Cuevas-Díaz Duran2, Adrian Ledesma-Beiza1, Cynthia Sámano1, Thalía Estefanía Sánchez-Correa3, Ernesto Soto-Reyes1,*

    BIOCELL, DOI:10.32604/biocell.2026.075061

    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 >

  • Open Access

    ARTICLE

    Integrated WGCNA and Experimental Validation Reveals LINC00595 as Necroptosis-Regulating lncRNAs in Prostate Cancer

    Kai Tang1, Shengxing Lu1, Cuie He2, Ruozeng Rong1,*

    BIOCELL, DOI:10.32604/biocell.2026.072154

    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 >

  • Open Access

    ARTICLE

    Dexmedetomidine Protects Intestinal Mucosal Barrier via Activating the α7-nAChR-GDNF in Enteric Glial Cells

    YUANHONG MAO#, YUNLAN YANG#, KUN YANG§, YONGQIANG SUN, KUN YANG*,,*

    BIOCELL, DOI:10.32604/biocell.2026.075138

    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 >

  • Open Access

    ARTICLE

    sIL-2RA Exacerbates Multiple Sclerosis by Activating Microglia and Upregulating Fc Receptors on Microglia

    JINGFEI SHI#, YI DING#, HUI LU*

    BIOCELL, DOI:10.32604/biocell.2026.073956

    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 >

  • Open Access

    ARTICLE

    Melatonin Ameliorates Hippocampal Excitotoxicity and Neuroinflammation in Permanent MCAO by Targeting NMDA/AMPA Receptors and the NLRP3 Inflammasome via Nrf2/PPARγ/JNK/NF-κB Crosstalk

    Abdullah Alattar1, Reem Alshaman1, Fawaz E. Alanazi1, Yusuf S. Althobaiti2, Ghareb M. Soliman3, Waleed Salman Khubrni1, Howaida S. Ali4, Fawad Ali Shah5,6,*

    BIOCELL, DOI:10.32604/biocell.2026.074865

    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 > Graphic Abstract

    Melatonin Ameliorates Hippocampal Excitotoxicity and Neuroinflammation in Permanent MCAO by Targeting NMDA/AMPA Receptors and the NLRP3 Inflammasome via Nrf2/PPAR<b>γ</b>/JNK/NF-<b>κ</b>B Crosstalk

  • Open Access

    REVIEW

    The Immune-Centric Revolution in the Treatment of Musculoskeletal Disease: Autologous PBMNC and PRP-PBMNC Enriched—A Narrative Review

    ANDREA DE MATTHAEIS1, LAURA REHAK2,*, MARIA BIANCHI3, ROSSANA PUTZULU3, NICOLA PICCIRILLO3,4, GIULIO MACCAURO1

    BIOCELL, DOI:10.32604/biocell.2026.073783

    Abstract For over two decades, mesenchymal stem cells (MSCs) have been recognised as the cornerstone of orthobiologic treatments for musculoskeletal diseases. However, clinical evidence increasingly indicates that MSC engraftment in inflamed tissues is minimal and transient, with effects mainly driven by paracrine and immunomodulatory mechanisms induced by macrophage efferocytosis. This evolving paradigm emphasises the immune system as the central orchestrator of tissue repair. Peripheral blood mononuclear cells (PBMNCs) have emerged as potent effectors of regenerative inflammation, mediating apoptotic cell clearance through efferocytosis, facilitating the transition of macrophages from pro-inflammatory (M1) to reparative (M2) phenotypes, and releasing… More >

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