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  • Open Access

    ARTICLE

    RP3-340N1.2 Knockdown Suppresses Proliferation and Migration by Downregulating IL-6 in Non-Small Cell Lung Cancer

    Hang Zhang1,#, Meng-Yuan Chu1,#, Guohui Lv1, You-Jie Li1, Xuhang Liu2, Fei Jiao1,*, Yun-Fei Yan1,*

    BIOCELL, DOI:10.32604/biocell.2025.068322

    Abstract Objectives: Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality, with limited understanding of lncRNA-driven mechanisms in tumor progression. This study aimed to identify differentially expressed lncRNAs in NSCLC tissues and elucidate the functional role of the significantly upregulated RP3-340N1.2 in promoting malignancy. Methods: RNA sequencing was used to screen dysregulated lncRNAs. RP3-340N1.2 was functionally characterized via gain/loss-of-function assays in NSCLC cells, assessing proliferation, migration, and macrophage polarization. Mechanisms of interleukin 6 (IL-6) regulation were explored using cytokine profiling, Actinomycin D assays, and RNA Immunoprecipitation (RIP) assays to study RP3-340N1.2 interactions with… More >

  • Open Access

    ARTICLE

    Immunoregulatory Subpopulations of iNKT Cells and Myeloid-Derived Suppressor Cells in Chronic Lymphocytic Leukemia: Implications for Disease Progression and Immune Evasion

    Przemysław Piwowarczyk1, Justyna Woś1, Agata Szymańska1, Sylwia Chocholska2, Waldemar Tomczak2, Jacek Roliński1, Agnieszka Bojarska-Junak1,*

    BIOCELL, DOI:10.32604/biocell.2025.074128

    Abstract Objectives: Chronic lymphocytic leukemia (CLL) is characterized by progressive immune dysregulation. Invariant natural killer T (iNKT) cells support immune surveillance, but the clinical relevance of their regulatory subsets remains unclear. FoxP3+ regulatory iNKT cells (iNKTreg) and E4BP4+IL-10+ (iNKT10) cells may reflect immunoregulatory changes associated with disease progression. The study aimed to quantify circulating iNKTreg and iNKT10 subsets and monocytic myeloid-derived suppressor cells (M-MDSCs) in treatment-naïve CLL patients and evaluate their associations with disease characteristics and time to first treatment (TTFT). Methods: Peripheral blood samples from 60 untreated CLL patients and 20 healthy donors were analyzed by… More >

  • Open Access

    ARTICLE

    Lithospermic Acid Promotes Osteoblast Proliferation and Differentiation through the Wnt/β-Catenin Signaling Pathway

    Jianfeng Wang#, Zhongqing Hu#, Jiandong Guo, Xin Jin, Lei Cai, Jian Li, Jinxi Zhang*, DONGAN HE*

    BIOCELL, DOI:10.32604/biocell.2025.072227

    Abstract Objectives: Therapeutic strategies for enhancing bone regeneration and combating osteoporosis remain a significant unmet medical need. This study aims to elucidate Lithospermic acid (LA)’s regulatory effects on osteoblast proliferation and differentiation, investigating its viability as a bone-healing agent. Methods: This study employed various cellular and molecular biology experiments to assess the effects of LA on the viability, proliferation, cell cycle, apoptosis, differentiation, mineralization, and migration of MC3T3-E1 osteoblasts. Immunofluorescence and Western blot analyses were conducted to detect the expression of proteins related to the Wnt/β-catenin signaling pathway, investigating the regulatory mechanisms by which LA promotes… More > Graphic Abstract

    Lithospermic Acid Promotes Osteoblast Proliferation and Differentiation through the Wnt/β-Catenin Signaling Pathway

  • Open Access

    REVIEW

    Molecular Mechanisms and Signaling Pathways of Myocardial Ischemia: A Multidimensional Analysis from Energy Metabolism to Cell Death

    YIWEI HAO1,#, YAODONG PING2,#, YAN YANG3, CHENG QU3, YUAN CHEN1, XUEYAN JIANG1, RONG FU1, HAILONG ZHAO4,*, LEI YU4,*

    BIOCELL, DOI:10.32604/biocell.2025.074863

    Abstract Myocardial ischemia, a core pathological process underlying diverse cardiovascular diseases such as coronary artery disease, poses a severe threat to global human health by frequently leading to acute myocardial infarction, heart failure, and even sudden cardiac death. A comprehensive understanding of its intricate underlying pathogenic mechanisms is not only crucial for developing effective therapeutic strategies but also essential for accelerating the translation of basic research findings into clinical practice. However, the complex regulatory networks that drive myocardial ischemia remain to be systematically clarified. These networks encompass the intricate interactions among multiple pathological processes, including energy… More >

  • Open Access

    REVIEW

    Targeting Protein Arginine Deiminases in Rheumatoid Arthritis: Pathophysiology and Therapeutic Progress

    Yung-Chieh Huang1,2,3, Wen-Chien Cheng4,5, Ya-Hsuan Chao6, Tzu-Ting Chen7,*, Chi-Chen Lin8,9,10,11,*

    BIOCELL, DOI:10.32604/biocell.2025.072732

    Abstract Protein arginine deiminases (PADs) are key enzymes in the development of rheumatoid arthritis (RA), catalyzing the conversion of arginine to citrulline in a process called citrullination. This post-translational modification is crucial to RA pathogenesis as it creates neo-antigens that trigger the production of anti-citrullinated protein antibodies (ACPAs). These ACPAs are highly specific to RA and often appear before clinical symptoms, making them valuable biomarkers for diagnosis and prognosis. Beyond ACPA production, PADs, particularly PAD4, play a vital role in forming neutrophil extracellular traps (NETs). NETs contribute to inflammation and joint damage, further highlighting the importance… More > Graphic Abstract

    Targeting Protein Arginine Deiminases in Rheumatoid Arthritis: Pathophysiology and Therapeutic Progress

  • Open Access

    REVIEW

    Understanding Endoplasmic Reticulum Stress as a Central Driver of Atherosclerosis

    Alessio L. Ravani1, Michael I. Bukrinsky2, Anastasia V. Poznyak3,*

    BIOCELL, DOI:10.32604/biocell.2025.074266

    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 >

  • Open Access

    REVIEW

    Cellular and Molecular Insights into the Pathophysiology of Obesity-Related Asthma

    HUAN ZHOU1, JIAMI JIANG2, YUQING ZOU1, JIAHUI ZHANG1,*, ZHIWEI YU3,*

    BIOCELL, DOI:10.32604/biocell.2025.073989

    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 >

  • Open Access

    ARTICLE

    Cellular Knockdown of SELENOM Promotes Apoptosis Induction in Human Glioblastoma (A-172) Cells via Redox Imbalance

    Egor A. Turovsky*, Elena G. Varlamova

    BIOCELL, DOI:10.32604/biocell.2025.073728

    Abstract Objectives: Glioblastoma multiforme (GBM) is highly resistant to apoptosis. This study investigates the role of Selenoprotein M (SELENOM), a redox-regulating protein, in the response of human glioblastoma A-172 cells to staurosporine (STS) and hyperthermia. Methods: A stable SELENOM-knockdown (SELENOM-KD) cell line was created. We measured reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm), cell death, and apoptotic gene expression. Results: SELENOM-KD increased basal ROS levels and induced mitochondrial dysfunction. It sensitized cells to STS-induced apoptosis, enhancing the upregulation of pro-apoptotic genes. Conversely, under hyperthermia (42°C), SELENOM-KD cells exhibited significant thermoresistance, with 52% survival vs. 99% death More >

  • Open Access

    ARTICLE

    Integrative Analysis of scRNA-Seq and Bulk RNA-Seq Reveals Novel Transcription Factor Regulating Endothelial Heterogeneity Induced by Lrg1 Following Cerebral Ischemia-Reperfusion

    SHAOFENG XIONG1,2, WENKAI LV3, GUOSHENG CAO4, LONGSHENG FU1, WEN LIU3, MENGFAN LEI2, YANNI LV1,5,*

    BIOCELL, DOI:10.32604/biocell.2025.073401

    Abstract Objective: Leucine-rich alpha-2 glycoprotein 1 (Lrg1) could regulate diverse cells in cerebral ischemia-reperfusion. Our study seeks to uncover Lrg1’s impact on endothelial cell heterogeneity via differentiation pathways and transcription factors. Method: The CSOmap model measured cell-to-brain-center distances using single-cell RNA sequencing (scRNA-seq) data in middle cerebral artery occlusion reperfusion (MCAO/R). Monocle2 mapped endothelial differentiation paths. Gene set enrichment analysis (GSEA) analyzed endothelial subcluster variations. Database searches revealed a zinc finger MIZ-type containing 1 protein-frizzled 3 (Zmiz1-Fzd3) promoter interaction. Endothelial cells were transfected with a Fzd3 promoter-luciferase plasmid. Polymerase chain reaction (PCR) and western blotting assessed… More >

  • Open Access

    REVIEW

    Mitochondrial Dysfunction as a Pathophysiological Bridge between Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease

    Congwei You1,#, Anwen Yin2,#, Jia Xia3, Le Zhang4,*, Xiaolei Wang1,*, Yutong Hou4,*

    BIOCELL, DOI:10.32604/biocell.2025.072971

    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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