BIOCELL, Vol.50, Suppl.4, pp. 1-36, 2026

Abstract This article has no abstract. More >

BIOCELL, Vol.50, Suppl.3, pp. 1-31, 2026

Abstract This article has no abstract. More >

BIOCELL, Vol.50, Suppl.2, pp. 1-40, 2026

Abstract This article has no abstract. More >

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 >

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 >

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 >

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 >

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

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 >

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

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 > Graphic Abstract

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

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 >