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Mihaela Jurdana^1,*, Lovro Ziberna^2,3

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.079591 - 27 July 2026
Abstract Obesity and metabolic syndrome promote malignancies through chronic inflammation and sustained activation of insulin and insulin-like growth factor-1 (IGF-1) signaling. Skeletal muscle is central to this tumor-promoting milieu because it governs insulin-stimulated glucose disposal, lipid oxidation, and endocrine crosstalk. This narrative review explores whether melatonin signaling in skeletal muscle, particularly via melatonin receptor 2 (MT₂), represents a modifiable node within the obesity–cancer axis. Experimental evidence indicates that melatonin activates MT₂-linked Gi/o and calcium-sensitive pathways converging on phosphoinositide 3-kinase–protein kinase B (PI3K–Akt), extracellular signal-regulated kinases (ERK), and calcium/calmodulin-dependent protein kinase II–adenosine monophosphate-activated protein kinase–peroxisome proliferator-activated receptor gamma More >

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637

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Deborah Joyce¹, Wan Muhammad Farhan Syafiq Wan Mohd Nor², Ivy Chung², Amira Hajirah Abd Jamil¹, Nur Akmarina Mohd Said^1,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.077378 - 27 July 2026
Abstract Non-coding RNAs (ncRNAs) and cholesterol metabolism have independently been recognized as critical regulators of cancer progression. NcRNAs modulate various aspects of cancer cell behaviour, including metabolic reprogramming, proliferation, migration, and intercellular communication. Concurrently, dysregulated cholesterol metabolism has emerged as a hallmark of cancer, influencing tumour growth, immune evasion, chemoresistance, and metastasis. While numerous studies have explored the role of ncRNAs like long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in modulating cholesterol metabolism within either cancer cells or immune cells, the mechanism of their action largely depends on the involvement of microRNAs (miRNAs). However, the… More >

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1486

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535

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Zhiqing Hu¹, Lisha Ma², Weili Zhu^2,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.077860 - 27 July 2026
（This article belongs to the Special Issue: Novel Targeted Therapy in Oncology)
Abstract Ovarian cancer (OC) is the most lethal gynecologic malignancy. The current first-line treatment still relies primarily on cisplatin-based chemotherapy, yet cisplatin resistance strongly predicts poor patient prognosis. Cuproptosis is a newly identified cell death modality driven by copper overload and impaired mitochondrial respiration. This review outlines the core molecular mechanisms of cuproptosis and examines its complex association with cisplatin resistance in ovarian cancer. Their interplay involves shared transport systems. In cisplatin-resistant ovarian cancer cells, copper influx transporter Copper Transporter 1 (CTR1) downregulation and efflux transporter ATPase copper transporting alpha/beta polypeptide (ATP7A/B) upregulation reduce the intracellular… More >

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924

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Babu Santha Aswani^1,#, Bethsebie Lalduhsaki Sailo^1,#, Young Yun Jung^2,#, Sosmitha Girisa¹, Mangala Hegde¹, Mohammed S Alqahtani^3,4, Mohamed Abbas⁵, Hassan Ali Almubarak⁶, Anupam Bishayee⁷, Kwang Seok Ahn^2,*, Ajaikumar B. Kunnumakkara^1,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.073397 - 27 July 2026
（This article belongs to the Special Issue: Natural Product-Based Anticancer Drug Discovery)
Abstract Despite the advancements achieved in chemotherapy, cancer continues to remain a formidable and lethal global threat, ranking as the second leading cause of death worldwide. The development of chemoresistance poses a significant hurdle in cancer treatment. Nonetheless, a therapeutic strategy known as chemosensitization has emerged to counteract cancer cell resistance, wherein the efficacy of one drug is augmented by another. Accumulating evidence suggests that natural products have attracted considerable attention in the cancer therapeutic realm due to their ability to combat multidrug resistance with minimal side effects. Ginsenosides, triterpene saponins extracted from Panax ginseng, have demonstrated… More >

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701

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Yibing Wang¹, Xingbo Wu¹, Yifei Shen¹, Xiayi Wang¹, Chun Hung Chu², Irene Shuping Zhao^2,3, Xueqi Gan^1,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.079089 - 27 July 2026
（This article belongs to the Special Issue: Modulation of Inflammation, Oxidative Stress, and Mitochondrial Function: Therapeutic Perspectives Across Diseases)
Abstract Periodontitis is a prevalent inflammatory disease characterized by the progressive destruction of tooth-supporting tissues. Its pathogenesis remains incompletely understood, but accumulating evidence highlights mitochondrial dynamics imbalance and oxidative stress as interconnected drivers. However, comprehensive reviews elucidating the molecular basis of this interaction are lacking. Therefore, this review aims to clarify the crosstalk between mitochondrial dynamics dysregulation and oxidative stress, and how this bidirectional interaction contributes to periodontal tissue destruction. This review first provides an overview of mitochondrial dynamics and the mechanisms of oxidative stress. We then contextualize these processes within periodontitis, detailing the dual role More >

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1682

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701

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Dominick Shoha^#, David Lei^#, Tyler Truong, Sophia Strukel, Elliot Enshaie, Vikrant Rai^*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.078846 - 27 July 2026
（This article belongs to the Special Issue: Unraveling the Interplay of Molecular and Cellular Mechanisms between Diabetes and Non-communicable Diseases )
Abstract Diabetes, inflammation, and neurodegeneration, particularly Alzheimer’s disease (AD), are deeply interconnected (brain diabetes). Type 2 diabetes mellitus (T2DM) acts as a significant risk factor for neurodegenerative diseases like Alzheimer’s (AD) and Parkinson’s (PD) by inducing chronic inflammation, oxidative stress, and metabolic dysfunction. Hyperglycemia drives neuroinflammation and damages the blood-brain barrier (BBB), exacerbating cognitive decline and neuronal loss. Chronic inflammation acts as a central bridge, linking high blood sugar, insulin resistance, and metabolic dysfunction in the brain to the buildup of amyloid plaques, tau tangles, and neuronal damage due to shared insulin signaling issues in the More >

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594

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Mohammad Muzaffar Mir^1,*, Rashid Mir^2,3, Badr A. Alsayed⁴, Mohammed M. Jalal³, Malik A. Altayar³, Hanan M. Aljammaz⁵, Zinab Alatawi⁶, Khalid A. Alfifi², Basmah M. Alenzi⁷, Mohammad Tanveer Khaji⁸, Umair Ismail⁹, Ghada Mohamed^10,11, Nada Zai Sageer¹², Abdullatif Taha Babakr¹³, Saba M. Mir¹⁴, Ulfat Jan¹⁵

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.077540 - 27 July 2026
Abstract The tuberculosis (TB) epidemic continues to be one of the largest public health challenges affecting people globally, especially due to late diagnosis, disease monitoring, and prognosis. Currently used diagnostic tools have variable sensitivity and accessibility, and many have limited ability to differentiate between latent and active TB. In case of TB, exosomes from cells infected with Mycobacterium tuberculosis (M. tuberculosis) have disease-specific antigens, microRNAs, and other molecular components, which make them potential diagnostic and prognostic biomarkers. This review focuses on previously published literature regarding the role of exosomes and exosomal antigens in TB screening and prognostication. It… More >

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680

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Zebiao Liu^1,#, Xuebing Zhan^1,#, Mingquan Chen¹, Junxi Lai², Wenli Zhao^1,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.081173 - 27 July 2026
Abstract Background: Immunosuppression contributes to breast cancer treatment failure, yet Cluster of Differentiation 74 (CD74) function in macrophages remains unclear. This study investigated how CD74 influences M1 macrophage polarization and its functional and expression profiles in breast cancer. Methods: We used bioinformatics analysis combined with in vitro cell experiments. The expression of CD74 in THP-1-derived M1 macrophages induced by Lipopolysaccharide/Interferon-gamma (LPS/IFN-γ) was knocked down by shRNA. Polarization markers were detected by WB, qPCR, and flow cytometry. Cytokines were detected by Enzyme-Linked Immunosorbent Assay (ELISA). The phagocytosis and killing effect of macrophages on MCF-7 cells were evaluated by a… More >

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383

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Bin Lian^1,2,#, Na You^2,3,#, Jingyu Wang⁴, Cong Wang⁴, Yunjie Wen², Jiandong Wang^5,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.081166 - 27 July 2026
Abstract Background: Rho GTPase-activating protein 40 (ARHGAP40), downregulated in various tumors, including basal cell carcinoma, has an unclear role in colorectal cancer (CRC). This study aimed to elucidate the function and clinical significance of ARHGAP40 in CRC. Methods: ARHGAP40 expression in CRC tissues was evaluated by immunohistochemistry and analyzed in relation to clinicopathological features and patient survival. Gain- and loss-of-function experiments were performed in CRC cell lines to assess cell proliferation, apoptosis, migration, and invasion. RNA sequencing, co-immunoprecipitation, Ras homolog gene family member A (RhoA) activation assays, and rescue experiments were conducted to explore the underlying mechanism. Results:… More >

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625

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235

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Lea Barbarić¹, Marina Oskomić¹, Anđela Horvat², Katja Ester², Nikolina Stojanović³, Ana Tomašić Paić¹, Mihaela Matovina^1,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.080282 - 27 July 2026
Abstract Objectives: Dipeptidyl peptidase 3 (DPP3) is a zinc metallopeptidase involved in peptide turnover and possibly in blood pressure and pain regulation. It also modulates oxidative stress response via the Kelch-like ECH-associated protein 1–nuclear factor erythroid 2-related factor 2 (KEAP1–NRF2) pathway. Although frequently upregulated in cancer, its role in carcinogenesis remains unclear. This study examined the effects of DPP3 knockdown (KD) and overexpression on migration, proliferation, and KEAP1–NRF2 pathway regulation in HeLa cells. Methods: We assessed the effects of DPP3-KD and overexpression on HeLa cell migration using a wound healing assay, and on NRF2 activity by measuring… More >

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771

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293

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Laura Schaltz^1,2, Simon Lassnig^1,2, Karola Schlote^1,2, Christian Schwerk³, Horst Schroten³, Nicole de Buhr^1,2,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.079046 - 27 July 2026
（This article belongs to the Special Issue: Neuroinflammation and Neuroprotection in CNS Diseases: From Mechanisms to Therapeutic Targets)
Abstract Objectives: Streptococcus suis (S. suis) is a worldwide occurring pathogen in pigs and humans that can cross the blood-cerebrospinal fluid barrier (BCSFB) to cause meningitis, while host neutrophils counter infection through mechanisms including the release of neutrophil extracellular traps (NETs). NET-formation involves the release of nuclear DNA with antimicrobial components, which can bind and kill bacteria. We aimed to characterize the host-pathogen interaction between S. suis and neutrophils within the CSF compartment, focusing on NET-formation. Methods: A 3D cell culture model of the porcine BCSFB was used by cultivating a porcine choroid plexus epithelial cell line (PCP-R) on filter… More >

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336

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Katerina Basharova^1,2,#,*, Anastasia Bezrukova^1,2,#, Alena Kopytova^1,2, Anna Lavrinova^1,2, Galina Baydakova³, Irina Miliukhina^1,4, Ekaterina Zakharova^1,3, Anton Emelyanov^1,2, Sofya Pchelina^1,2, Tatiana Usenko^1,2,*

BIOCELL, Vol.50, No.8, 2026, DOI:10.32604/biocell.2026.079585 - 27 July 2026
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms in Parkinson's Disease: Novel Targets and Biomarkers for Target Therapy)
Abstract Objectives: Synucleinopathies—Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA)—involve alpha-synuclein aggregation and lysosomal dysfunction. We conducted a longitudinal study of lysosomal hydrolase activities and lysosphingolipid levels in blood and PBMC-derived macrophages from patients, and assessed the effects of LRRK2 inhibition (MLi-2). Methods: Blood and PBMC-derived macrophages were collected from patients with idiopathic PD (iPD), DLB, MSA, and controls. Enzyme activities (GCase, ASMase, GLA, GALC) and lysosphingolipids (HexSph, LysoGb3, LysoSM) were measured. Autophagy markers (p62, LC3B-II) and cathepsin D (CTSD) were analyzed by western blot. Effects of MLi-2 were evaluated in macrophages. Results:… More >

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272

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Andrew Scarborough¹, Yvoni Kyriakidou¹, Derek C. Lee², Tomás Duraj², Thomas N. Seyfried², Isabella D. Cooper^1,*

BIOCELL, Vol.50, No.6, 2026, DOI:10.32604/biocell.2026.074152
（This article belongs to the Special Issue: Homeostasis of Mitochondria: Unraveling its Multifaceted Role in Health and Disease)
Abstract The global rise in chronic, non-communicable diseases (NCDs) is inextricably linked to metabolic dysfunction, with hyperinsulinaemia acting as a potent upstream driver of ageing and age-related disease. Some of the most burdensome diseases of our time, including type 2 diabetes, cardiovascular disease, cancer, and neurodegenerative conditions, such as Alzheimer’s disease (AD), are largely underpinned by insulin resistance as part of a broader system of metabolic and mitochondrial dysfunction. These pathologies are particularly pronounced in the developed world, where obesity and other lifestyle-related conditions are major contributors to disease burden and premature mortality. As an upstream… More >

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2074

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Stephanie Seneff^1,*, Greg Nigh², Anthony M. Kyriakopoulos^3,4

BIOCELL, Vol.49, No.9, pp. 1545-1572, 2025, DOI:10.32604/biocell.2025.066687
（This article belongs to the Special Issue: Cellular Mechanisms and Therapeutic Approaches in Protein Misfolding Diseases)
Abstract Deuterium is a heavy isotope of hydrogen, with an extra neutron, endowing it with unique biophysical and biochemical properties compared to hydrogen. The ATPase pumps in the mitochondria depend upon proton motive force to catalyze the reaction that produces ATP. Deuterons disrupt the pumps, inducing excessive reactive oxygen species and decreased ATP synthesis. The aim of this review is to develop a theory that mitochondrial dysfunction due to deuterium overload, systemically, is a primary cause of Parkinson’s disease (PD). The gut microbes supply deuterium-depleted short chain fatty acids (SCFAs) to the colonocytes, particularly butyrate, and… More >

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1493

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Russel J. Reiter^1,*, Ramaswamy Sharma^2,*, Walter Manucha³, Walter Balduini⁴, Doris Loh⁵, Demetrios A. Spandidos⁶, Alejandro Romero⁷, Vasiliki E. Georgakopoulou⁸, Wei Zhu⁹

BIOCELL, Vol.49, No.11, pp. 2033-2067, 2025, DOI:10.32604/biocell.2025.067661
（This article belongs to the Special Issue: Melatonin and Mitochondria: Exploring New Frontiers)
Abstract The development of cancer cell resistance to conventional treatments continues to be a major obstacle in the successful treatment of tumors of many types. The discovery of a highly efficient direct and indirect free radical scavenger, melatonin, in the mitochondrial matrix may be a factor in determining both the occurrence of cancer cell drug insensitivity as well as radioresistance. This relates to two of the known hallmarks of cancer, i.e., exaggerated free radical generation in the mitochondria and the development of Warburg type metabolism (glycolysis). The hypothesis elaborated in this report assumes that the high… More >

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1532

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Carmen Rubio^1,#, Norma Serrano-GarcíA^1,#, Elisa Taddei¹, Eduardo CastañEda², HéCtor Romo^1,3, MoiséS Rubio-Osornio^4,*

BIOCELL, Vol.49, No.8, pp. 1391-1412, 2025, DOI:10.32604/biocell.2025.066320
（This article belongs to the Special Issue: Mitochondrial Dynamics and Oxidative Stress in Disease: Cellular Mechanisms and Therapeutic Targets)
Abstract Rotenone is a lipophilic herbicide extensively utilized in experimental neurodegenerative models because of its capacity to disrupt complex I of the mitochondrial electron transport chain. This inhibition results in reduced ATP synthesis, elevated reactive oxygen species (ROS) formation, and mitochondrial malfunction, which instigates oxidative stress and cellular damage, critical elements in neurodegenerative disorders like Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Alzheimer’s disease (AD). In addition to causing direct neuronal injury, rotenone significantly contributes to the activation of glial cells, specifically microglia and astrocytes. Activated microglia assumes a proinflammatory (M1) phenotype, distinguished by the… More >

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2127

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LIUJIE CHEN^1,#, LILI DUAN^1,2,#, JIA LI^1,2, JUN CHEN^1,2, DUANFANG LIAO³, NONGYUE HE⁴, KAI LI^1,3, ZHENG HU^1,2,*

BIOCELL, Vol.49, No.1, pp. 21-43, 2025, DOI:10.32604/biocell.2024.056698
Abstract Nucleic acid analysis is a key technique that enables accurate detection of various microorganisms. Conventional nucleic acid testing typically requires access to specialized laboratories, equipment, and trained personnel, which hinders the widespread use of on-site testing for DNA and RNA targets. However, integrating gene editing technology with traditional nucleic acid detection methods, especially isothermal amplification technology, can help overcome the limitations associated with on-site testing. This combination can accomplish precise and swift detection of nucleic acid sequences, offering a robust tool for on-site detection. The Clustered Regularly Interspaced Short Palindromic Repeats/CRISPR-associated proteins (CRISPR/Cas) technology, which More >

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4341

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1837

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Iman Ezzat, Marisa Zallocchi^*

BIOCELL, Vol.49, No.5, pp. 789-811, 2025, DOI:10.32604/biocell.2025.062325
（This article belongs to the Special Issue: Extracellular Matrix in Development and Disease)
Abstract Integrins are heterodimeric transmembrane receptors that mediate bidirectional interactions between the intracellular cytoskeletal array and the extracellular matrix. These interactions are critical in tissue development and function by regulating gene expression and sustaining tissue architecture. In humans, the integrin family is composed of 18 alpha (α) and 8 beta (β) subunits, constituting 24 distinct αβ combinations. Based on their structure and ligand-binding properties, only a subset of integrins, 8 out of 24, recognizes the arginine-glycine-aspartate (RGD) tripeptide motif in the native ligand. One of the major RGD binding integrins is integrin alpha 8 beta 1 More >

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4145

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1183

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VIRAAJ VISHNU PRASAD, JENNIFER SALLY SAMSON, VENKATACHALAM DEEPA PARVATHI^*

BIOCELL, Vol.48, No.5, pp. 693-706, 2024, DOI:10.32604/biocell.2024.048776
（This article belongs to the Special Issue: Exploring the Cellular Mechanisms of Neurodegenerative Diseases)
Abstract Physical activity and exercise have several beneficial roles in enhancing both physiological and psychological well-being of an individual. In addition to aiding the regulation of aerobic and anaerobic metabolism, exercise can stimulate the synthesis of exerkine hormones in the circulatory system. Among several exerkines that have been investigated for their therapeutic potential, Brain-derived neurotrophic factor (BDNF) is considered the most promising candidate, especially in the management of neurodegenerative diseases. Owing to the ability of physical activity to enhance BDNF synthesis, several experimental studies conducted so far have validated this hypothesis and produced satisfactory results at More >

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1357

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YARA ALZGHOUL, HALA J. BANI ISSA, AHMAD K. SANAJLEH, TAQWA ALABDUH, FATIMAH RABABAH, MAHA AL-SHDAIFAT, EJLAL ABU-EL-RUB^*, FATIMAH ALMAHASNEH, RAMADA R. KHASAWNEH, AYMAN ALZU’BI, HUTHAIFA MAGABLEH

BIOCELL, Vol.48, No.4, pp. 559-569, 2024, DOI:10.32604/biocell.2024.048056
（This article belongs to the Special Issue: Perspectives on Stem Cells and Regenerative Medicine)
Abstract Mesenchymal stem cells (MSCs) are ideal candidates for treating many cardiovascular diseases. MSCs can modify the internal cardiac microenvironment to facilitate their immunomodulatory and differentiation abilities, which are essential to restore heart function. MSCs can be easily isolated from different sources, including bone marrow, adipose tissues, umbilical cord, and dental pulp. MSCs from various sources differ in their regenerative and therapeutic abilities for cardiovascular disorders. In this review, we will summarize the therapeutic potential of each MSC source for heart diseases and highlight the possible molecular mechanisms of each source to restore cardiac function. More >

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3947

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1511

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Virna Margarita Martín Giménez¹, SebastiáN GarcíA MenéNdez^2,3, Luiz Gustavo A. Chuffa⁴, Vinicius Augusto SimãO⁴, Russel J. Reiter⁵, Ramaswamy Sharma⁶, Walter Balduini⁷, Carla Gentile⁸, Walter Manucha^2,3,*

BIOCELL, Vol.49, No.12, pp. 2245-2282, 2025, DOI:10.32604/biocell.2025.071830
（This article belongs to the Special Issue: Melatonin and Mitochondria: Exploring New Frontiers)
Abstract Neurodegenerative diseases (NDs) such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS) are characterized by progressive neuronal loss, which is closely linked to mitochondrial dysfunction. These pathologies involve a complex interplay of genetics, protein misfolding, and cellular stress, culminating in impaired energy metabolism, an increase in reactive oxygen species (ROS), and defective mitochondrial quality control. The accumulation of damaged mitochondria and dysregulation of pathways such as the Integrated Stress Response (ISR) are central to the pathogenesis of these conditions. This review explores the critical relationship between mitochondrial stress… More >

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1014

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Kyung-Wan Baek^1,2,#, Jinkyung Cho^3,#, Ji Hyun Kim⁴, Ji-Seok Kim^1,2,*

BIOCELL, Vol.49, No.8, pp. 1339-1362, 2025, DOI:10.32604/biocell.2025.064916
（This article belongs to the Special Issue: Cellular and Molecular Mechanisms of Exercise in Aging and Chronic Disease)
Abstract Chronic kidney disease (CKD) affects a significant fraction of the global population and is closely associated with elevated cardiovascular risk and poor clinical outcomes. Its pathophysiology entails complex molecular and cellular disturbances, including reduced nitric oxide bioavailability, persistent low-grade inflammation, oxidative stress, endothelial dysfunction, altered mineral metabolism, genetic predispositions, and uremic toxin accumulation. As current pharmacological treatments provide only partial risk reduction, complementary approaches are imperative. Exercise training, both aerobic and resistance, has emerged as a potent non-pharmacological intervention targeting these underlying molecular pathways. Regular exercise can enhance nitric oxide signaling, improve antioxidant defenses, attenuate… More >

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