Experimental Cell Research[JOURNAL]
Sun
200 papers
Retraction notice to "SND1 facilitates the invasion and migration of cervical cancer cells by Smurf1-mediated degradation of FOXA2" [Exp. Cell Res. 388 (2020) 111809].
Zhan F, Zhong Y, Qin Y … +3 more , Li L, Wu W, Yao M
Exp Cell Res · 2026 Jun · PMID 41966886 · Publisher ↗
Abstract loading — click title to view on PubMed.
Epigenetic silencing of GPD1 by HDAC2 via H3K9 deacetylation promotes head and neck squamous cell carcinoma progression.
Xue L, Tang W, Zhou M … +2 more , Ling Q, Zhou J
Exp Cell Res · 2026 Jun · PMID 41962619 · Publisher ↗
BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) remains a lethal malignancy with its pathogenic mechanisms incompletely unraveled. This study interrogates the role of the HDAC2-GPD1 axis in driving HNSCC progre...
BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) remains a lethal malignancy with its pathogenic mechanisms incompletely unraveled. This study interrogates the role of the HDAC2-GPD1 axis in driving HNSCC progression. METHODS: HDAC2 and GPD1 expression was analyzed in HNSCC tissues (IHC) and cell lines (RT-qPCR). TCGA-HNSCC dataset (520 tumors, 44 normal controls) was used for bioinformatics analysis of gene expression, correlation, and prognostic value. Stable HNSCC cell lines with HDAC2/GPD1 overexpression or knockout were established via lentiviral infection. CCK-8, Transwell, wound healing, and flow cytometry were performed to assess cell proliferation, invasion, migration and apoptosis in vitro. ChIP assays were conducted to verify the binding of HDAC2 to the GPD1 promoter and the H3K9ac modification of GPD1. Nude mice were implanted with modified FaDu cells to assess tumor growth via tumor measurements and HE analyses. RESULTS: HDAC2 was upregulated while GPD1 was downregulated in HNSCC tissues and cell lines, consistent with TCGA data. TCGA analysis showed an inverse correlation between HDAC2 and GPD1 (R = -0.2, P = 2.8e-06) and a poor prognostic trend in the GPD1/HDAC2 subgroup. Lentivirus-mediated HDAC2 overexpression or GPD1 knockdown in HNSCC cells enhanced proliferation, invasion, and migration, while suppressing apoptosis. Conversely, GPD1 overexpression reversed these malignant phenotypes. ChIP assays confirmed HDAC2 binding to the GPD1 promoter, reducing H3K9 acetylation to repress GPD1 transcription. In vivo, Santacruzamate A (SCA) (an HDAC2 inhibitor) significantly inhibited xenograft tumor growth and restored GPD1 expression. Modified FaDu cell-derived xenografts showed that GPD1 knockdown accelerated tumor growth, which was inhibited by SCA. CONCLUSIONS: HDAC2 represses GPD1 via H3K9 deacetylation to promote HNSCC progression, highlighting the HDAC2-GPD1 axis as a potential therapeutic target.
Sgp130Fc regulates IL-6/JAK2/STAT3 trans-signaling pathway in rat vocal fold fibroblast activation.
Gao M, Li X, Wang H … +3 more , Lin Y, Hu R, Xu W
Exp Cell Res · 2026 Jun · PMID 41962618 · Publisher ↗
Acute vocal fold injury activates rat vocal fold fibroblasts (VFFs) and upregulates IL-6 expression. We investigated whether soluble gp130Fc (sgp130Fc) modulates IL-6 trans-signaling via the JAK2/STAT3 pathway. We establ...
Acute vocal fold injury activates rat vocal fold fibroblasts (VFFs) and upregulates IL-6 expression. We investigated whether soluble gp130Fc (sgp130Fc) modulates IL-6 trans-signaling via the JAK2/STAT3 pathway. We established a vocal fold injury model, isolated primary VFFs, and silenced JAK2 expression using siRNA. The cultured cells were then treated with exogenous IL-6 and/or sgp130Fc. We found that vocal fold injury activated VFFs, concomitant with a significant increase in IL-6 expression, and these alterations were reversed by JAK2 silencing. Treatment with exogenous IL-6 further enhanced the expression of COL-1, α-SMA, IL-6, and JAK2/STAT3 pathway components at both transcriptional and translational levels in VFFs, confirming its activating role in both transfected and non-transfected groups. Exogenous sgp130Fc regulates JAK2 signaling and attenuates the upregulation of COL-1, α-SMA and IL-6 protein expression and STAT3 phosphorylation levels induced by exogenous IL-6. JAK2 silencing partially reversed the activated VFF phenotype, concomitant with reduced mRNA and protein expression of COL-1, α-SMA, IL-6, and JAK2/STAT3 pathway components. Additionally, this intervention attenuated the regulatory effect of sgp130Fc on IL-6 trans-signaling. In conclusion, our data suggest involvement of IL-6 trans-signaling pathways during VFF activation. Exogenous sgp130Fc can inhibit IL-6 trans-signaling transduction and alleviate exogenous IL-6-induced VFF activation and STAT3 phosphorylation, and its effects may be dependent on JAK2 signaling. These insights position the IL-6 trans-signaling pathway as a critical regulator of VFF activation and suggest sgp130Fc as a potential therapeutic strategy for vocal fold fibrosis, while its applicability warrants further in vivo validation.
Mechanism of ginkgetin in inducing immunogenic cell death of gastric cancer cells by inhibiting the STAT3 signaling.
Li Q, Sun A
Exp Cell Res · 2026 Jun · PMID 41946410 · Publisher ↗
Gastric cancer (GC) ranks among the most prevalent and lethal malignancies worldwide. Conventional therapeutic modalities exhibit limited clinical efficacy and are accompanied by severe adverse effects. Consequently, the...
Gastric cancer (GC) ranks among the most prevalent and lethal malignancies worldwide. Conventional therapeutic modalities exhibit limited clinical efficacy and are accompanied by severe adverse effects. Consequently, there remains an urgent unmet clinical need for effective therapeutic strategies. Ginkgetin (Gin), a major biflavonoid compound isolated from the leaves of Ginkgo biloba L., has been demonstrated to exert anti-tumor activities against a variety of cancer types. Nevertheless, the biological effects and underlying mechanisms of ginkgetin in GC have rarely been reported. Therefore, the present study seeks to investigate the therapeutic potential and molecular mechanisms of ginkgetin in the management of GC. In vitro experiment, MTT assay, EdU assay, transwell assay, ELISA, and flow cytometry were employed to investigate the impacts of Gin on the proliferation, migration, apoptosis, mitochondrial damage, and immunogenic cell death (ICD) of GC cells. Subsequently, in vivo experiment, the immunomodulatory and anti-tumor activities of Gin were evaluated using ELISA and flow cytometry. Finally, network pharmacology and molecular docking analyses were performed to identify the core targets and pathways underlying Gin-mediated therapeutic effects against GC, with further validation conducted via vitro experiments. In vitro assays demonstrated that Gin potently suppressed the proliferation and migration of gastric cancer cells, promoted intracellular reactive oxygen species (ROS) production,and triggered cancer cell apoptosis. Most notably, Gin was capable of eliciting ICD in gastric cancer cells. In vivo experimental results revealed that Gin could activate anti-tumor immune responses, reverse the immunosuppressive tumor microenvironment (TME), thereby boosting the overall anti-tumor immune response and ultimately inhibiting tumor progression. Collectively, network pharmacology analyses and in vitro validation experiments indicated that Gin exerts its therapeutic efficacy against gastric cancer by blocking the phosphorylation of STAT3. By targeting STAT3 to trigger ICD in gastric cancer cells, ginkgetin activates anti-tumor immune responses and reverses the immunosuppressive TME, thereby providing novel insights into the pharmacological mechanisms underlying its therapeutic effects against GC.
Pituitary adenoma-induced IGF-I triggers increased proliferation and tumorigenic potential of thyroid cells by suppressing KLLN via MET/TP53 axis.
Guo X, Yang L, Zhong J … +9 more , Wu B, Yang C, Wu J, Wang X, Xie Y, Zhang R, Zhang J, Du Q, Chen Z
Exp Cell Res · 2026 Jun · PMID 41941934 · Publisher ↗
Pituitary adenoma (PA) is a chronic endocrine disease leading to various physiological abnormities. Our previous study has revealed that PA would result in thyroid diseases including goiter and thyroid cancer, which are...
Pituitary adenoma (PA) is a chronic endocrine disease leading to various physiological abnormities. Our previous study has revealed that PA would result in thyroid diseases including goiter and thyroid cancer, which are caused by increased proliferation and tumorigenic potential of thyroid cells. However, the mechanism of PA inducing thyroid diseases remains unclear. Our recent study has indicated that insulin-like growth factor I (IGF-I) might be positively correlated with thyroid diseases in PA patients. Therefore, the primary aim of this study was to investigate the mechanism of PA-induced IGF-I triggering increased proliferation and tumorigenic potential of thyroid cells. In this study, cell proliferation was detected using CCK-8 assay, clone formation ability was identified by clone formation assay, and nude mice xenograft tumor model was established to determine the tumorigenicity of IGF-I-treated thyroid cells in vivo. The current study confirms that IGF-I is positively associated with thyroid diseases in PA patients. Besides, IGF-I is found to promote thyroid cell proliferation and increase tumorigenic potential of thyroid cells by decreasing Killin (KLLN). Moreover, IGF-I declines KLLN by activating MET proto-oncogene, receptor tyrosine kinase (MET) in thyroid cells. Additionally, IGF-I-activated MET reduces KLLN by suppressing KLLN transcription via repressing tumor protein 53 (TP53) in thyroid cells. These findings uncover that the PA-dependent IGF-I/MET/TP53/KLLN signaling axis contributes to increased proliferation and tumorigenic potential of thyroid cells, which should provide potential therapeutic targets for thyroid diseases in PA.
Characterization of synaptopodin in striated and smooth muscles: isoform spectrum, expression patterns, localization and protein interactions.
Lohanadan K, Assent M, Linnemann A … +8 more , Qu C, Schänzer A, Heukamp L, Milting H, Kirfel G, Miner JH, Fürst DO, van der Ven PFM
Exp Cell Res · 2026 Jun · PMID 41941933 · Publisher ↗
Synaptopodin (SYNPO), founding member of the family of podin proteins, was mainly studied in the kidney and the brain. Here, SYNPO was initially described to be expressed in renal podocytes and the endoplasmic reticulum...
Synaptopodin (SYNPO), founding member of the family of podin proteins, was mainly studied in the kidney and the brain. Here, SYNPO was initially described to be expressed in renal podocytes and the endoplasmic reticulum (ER-)related spine apparatus in dendritic spines, respectively. More recently, SYNPO expression was also reported in epithelial cells, and database analyses even indicate ubiquitous expression, including high expression in striated and smooth muscle cells. Hrt (hard return) our analyses at RNA and protein levels confirm expression of distinct SYNPO variants in all striated and smooth muscle cell-containing organs analyzed and identify isoform-specific expression of SYNPO in human and mouse tissues. Immunostaining of tissue sections revealed diffuse localization at myofibrillar Z-discs in striated muscle fibers and at intercalated discs of cardiomyocytes. In skeletal muscle fibers, but also in cardiomyocytes, SYNPO partially colocalizes with longitudinal sarcoplasmic reticulum (SR-)associated STIM1. In smooth muscle cells, SYNPO shows a reticular distribution, compatible with potential co-distribution with the SR in these cells. In addition to previously reported interactions with actin and α-actinin, our protein interaction studies reveal a small region of SYNPO, homologous to the filamin C (FLNc)-binding region of SYNPO2, to bind FLNc. Transfection of SYNPO isoforms indicate close association with myofibrillar Z-discs in skeletal myotubes as well as stress fiber dense bodies and focal adhesions in smooth muscle cells. Our data identify strong expression of SYNPO variants in all muscle cell types, and indicate a role for SYNPO in the interaction between the actin cytoskeleton and the sarcoplasmic reticulum.
Methionine aminopeptidase 1D preserves myogenic cell integrity via maintaining mitochondrial activity.
Tsai CT, Hsu CF, Murakami R … +6 more , Takagaki Y, Uchibori H, Kaneko M, Hata K, Kano Y, Osana S
Exp Cell Res · 2026 Jun · PMID 41935813 · Publisher ↗
Mitochondria are essential organelles that regulate cellular energy production and homeostasis, and there are more than 40 resident proteases known to contribute to mitochondrial activity and dynamics. Among them, the mi...
Mitochondria are essential organelles that regulate cellular energy production and homeostasis, and there are more than 40 resident proteases known to contribute to mitochondrial activity and dynamics. Among them, the mitochondrial aminopeptidase methionine aminopeptidase 1D (Metap1D) is primarily involved in protein processing, including N-terminal methionine removal. Despite its potential significance, the role of Metap1D in myoblast proliferation and myogenic differentiation remains unclear. In this study, we investigated the function of Metap1D in C2C12 myoblasts, focusing on mitochondrial regulation, cell proliferation, and myogenic differentiation. Suppression of Metap1D by siRNA increased Pgc1α expression and mitochondrial content as well as mitochondrial membrane potential and intracellular ATP levels. Short-term knockdown of Metap1D enhanced cell proliferation with increased phosphorylation of the retinoblastoma protein, a key regulator of the cell cycle; however, prolonged suppression reduced proliferation. Furthermore, Metap1D knockdown reduced the expression of myogenic markers, including myogenin and myosin heavy chain, and was associated with impaired myogenic differentiation, accompanied by the formation of multinucleated myotubes with abnormal spherical morphology. These findings suggest that mitochondria-localized Metap1D is involved in the regulation of mitochondrial content and activity and is associated with the control of C2C12 myoblast proliferation and myogenic differentiation.
The role of MBD3 in cell biology and disease: Recent advances and future directions.
Meng J, Yang X, Luo H … +5 more , Liao Y, Wei P, Jian H, Huang A, Zhou W
Exp Cell Res · 2026 Jun · PMID 41933571 · Publisher ↗
MBD3 (mBD3, methyl-CpG binding domain protein 3) is a key epigenetic regulator that is involved in a wide range of biological processes including gene expression regulation, cell differentiation, and development. With th...
MBD3 (mBD3, methyl-CpG binding domain protein 3) is a key epigenetic regulator that is involved in a wide range of biological processes including gene expression regulation, cell differentiation, and development. With the realization of the importance of epigenetics in biological systems, the role of MBD3 in normal and abnormal conditions, especially with respect to cancer and neurodegenerative diseases, has received increasing attention. MBD3 affects the mechanisms of essential processes by regulating the binding of transcription factors and chromatin remodeling. Here we review the structure and functions of MBD3, its role in cell biology, the mechanisms of its action in different diseases, and future research directions, with the aim of increasing our understanding of MBD3 and its potential in clinical applications.
Zn-dependent modulation of the mitochondrial Ca uniporter underlies resveratrol-mediated protection against myocardial ischemia-reperfusion injury.
Xing B, Li X, Wang B … +6 more , Huang L, Wang Q, Chen X, Zheng H, He Y, Xi J
Exp Cell Res · 2026 Jun · PMID 41932596 · Publisher ↗
PURPOSE: This study aims to determine whether resveratrol (Res) regulates the mitochondrial calcium uniporter (MCU) in a Zn-dependent manner to influence mitochondrial biogenesis and dynamics, thereby alleviating myocard...
PURPOSE: This study aims to determine whether resveratrol (Res) regulates the mitochondrial calcium uniporter (MCU) in a Zn-dependent manner to influence mitochondrial biogenesis and dynamics, thereby alleviating myocardial ischemia-reperfusion injury (MIRI) and conferring cardioprotective effects. METHODS: H9c2 cardiomyocytes were cultured to establish an in vitro ischemia/reperfusion (I/R) model. Biochemical assays and transmission electron microscopy were used to assess cellular injury and mitochondrial ultrastructure after I/R. Protein structure prediction and molecular docking analyses were conducted to explore Res-protein interactions. Western blot, immunofluorescence staining, and RT-qPCR were performed to determine the expression of MCU, mitochondrial biogenesis and dynamics-related proteins. Confocal microscopy was used to measure mitochondrial membrane potential changes, and intracellular Zn and Ca fluorescence intensities. RESULTS: Compared with Control group, I/R significantly reduced myocardial viability, increased cytotoxicity, and decreased intracellular Zn levels, ATP content, and NAD/NADH ratio. The expression of mitochondrial biogenesis regulators (SIRT1, PGC-1α, NRF1, TFAM) and fusion-related proteins (OPA1, Mfn1, Mfn2) were downregulated, whereas fission-related proteins (Drp1, Fis1) were upregulated. MCU protein and mRNA levels were increased, alongside reduced PGC-1α/TFAM mRNA levels and decreased mitochondrial DNA copy number. In addition, MMP and Zn fluorescence intensities decreased, while Ca intensity increased. Res treatment attenuated I/R-induced cellular and mitochondrial injuries; however, the zinc chelator TPEN reversed these effects. Furthermore, MCU silencing by siRNA further enhanced the protective effects of Res. CONCLUSIONS: Resveratrol exerts cardioprotective effects against MIRI by increasing intracellular Zn to modulate MCU activity, thereby promoting mitochondrial biogenesis and fusion, inhibiting excessive fission, improving mitochondrial function, and ultimately attenuating MIRI.
Sirt1 deficiency promotes dynamic fibroblast-to-myofibroblast transition in ligamentum flavum hypertrophy via the Smad2/3 pathway.
Liu C, Li H, Fu J … +6 more , Liu C, Zheng F, Chen Y, Luo G, Li C, Zhai Y
Exp Cell Res · 2026 Jun · PMID 41932595 · Publisher ↗
BACKGROUND: Ligamentum flavum hypertrophy (LFH), a major pathological feature of lumbar spinal stenosis, is characterized by fibrosis and extracellular matrix (ECM) remodeling. However, the molecular mechanisms remain un...
BACKGROUND: Ligamentum flavum hypertrophy (LFH), a major pathological feature of lumbar spinal stenosis, is characterized by fibrosis and extracellular matrix (ECM) remodeling. However, the molecular mechanisms remain unclear. This study investigates the role of Sirtuin 1 (Sirt1), a NAD-dependent deacetylase, in regulating fibroblast-to-myofibroblast transition (FMT) in LFH. METHODS: Human LF samples and a rat LFH model were examined using histological, immunohistochemical, and molecular analyses. Single-cell RNA sequencing (scRNA-seq) was performed to explore LF cellular heterogeneity and identify fibrosis-related regulators. In vitro, Sirt1 activity was modulated pharmacologically and genetically to assess its role in fibroblast activation. Transcriptomic and bioinformatic analyses were used to identify downstream pathways, and lentiviral overexpression of Sirt1 in vivo was applied to evaluate therapeutic effects. RESULTS: scRNA-seq revealed fibroblasts as the dominant cell type in LFH and showed Sirt1 downregulation during fibrosis progression. Sirt1 inhibition enhanced FMT in ligamentum flavum cells, increasing α-SMA, Col-I, and Col-III expression via activation of the Smad2/3 signaling pathway. Conversely, Sirt1 overexpression mitigated LF fibrosis and improved sensory function in rats. CONCLUSIONS: Loss of Sirt1 promotes fibroblast-to-myofibroblast transition through Smad2/3 activation, while Sirt1 restoration alleviates LFH, suggesting Sirt1 as a promising therapeutic target for LF fibrosis.
EP300/NCOA1 complex drives glioma angiogenesis via H3K27 acetylation-dependent activation of VEGFA.
Yang S, Yao X, Lin X … +2 more , Yang D, Ying X
Exp Cell Res · 2026 Jun · PMID 41921814 · Publisher ↗
Angiogenesis is essential for glioma progression, yet the epigenetic mechanisms driving this process remain incompletely defined. In this study, we investigated the role of the histone acetyltransferase EP300 in regulati...
Angiogenesis is essential for glioma progression, yet the epigenetic mechanisms driving this process remain incompletely defined. In this study, we investigated the role of the histone acetyltransferase EP300 in regulating VEGFA expression and promoting endothelial activation. Using glioma cell lines with EP300 overexpression or knockdown, we found that EP300 markedly enhanced endothelial proliferation, invasion, and tube formation, while its silencing produced opposite effects. Mechanistic analyses revealed that EP300 increased H3K27 acetylation at the VEGFA promoter, thereby activating VEGFA transcription. Pharmacologic blockade of EP300 activity or VEGFA neutralization abolished these pro-angiogenic effects. Through integrative analysis of TCGA data and protein complex databases, NCOA1 was identified as a key EP300-associated cofactor. Co-immunoprecipitation and nuclear-cytoplasmic assays confirmed that EP300 forms a nuclear transcriptional co-activator complex with NCOA1, which stabilizes its nuclear localization and synergistically enhances VEGFA expression. Together, these findings identify EP300 as a central epigenetic regulator of glioma angiogenesis and highlight the EP300/NCOA1-VEGFA axis as a potential therapeutic target.
AGTPBP1 promotes breast cancer progression via the EVPL/ERK signaling axis.
Song H, Li H, Bian Y … +6 more , Song J, Yang C, Lu H, Zhang Y, Li P, Xiao R
Exp Cell Res · 2026 May · PMID 41905574 · Publisher ↗
BACKGROUND: The role of ATP/GTP binding protein 1 (AGTPBP1), a cytosolic carboxypeptidase, in oncogenesis remains largely unexplored. Although we previously identified its tumor-promoting function in pancreatic cancer, i...
BACKGROUND: The role of ATP/GTP binding protein 1 (AGTPBP1), a cytosolic carboxypeptidase, in oncogenesis remains largely unexplored. Although we previously identified its tumor-promoting function in pancreatic cancer, its expression pattern, biological function, and underlying mechanisms in breast cancer remain elusive. METHODS: AGTPBP1 expression and its clinical relevance in breast cancer were first assessed using public proteomic databases. Stable AGTPBP1 overexpression and knockdown models were established in the luminal A T47D and triple-negative MDA-MB-231 breast cancer cell lines to account for tumor heterogeneity. Malignant phenotypes were evaluated through a series of in vitro functional assays, including proliferation, colony formation, migration, and matrigel invasion assays. Mechanistic insights were gained by RNA-sequencing (with biological triplicates) and subsequent experimental validation, including rescue experiments. RESULTS: AGTPBP1 was significantly upregulated in breast cancer tissues. Functional studies demonstrated that AGTPBP1 overexpression markedly enhanced cell proliferation, colony formation, migration and invasion, whereas its knockdown suppressed these malignant behaviors. Transcriptomic profiling revealed that AGTPBP1 was critically involved in cell adhesion and cell-cell junction pathways. We identified envoplakin (EVPL), a core desmosomal protein, as a key downstream effector, whose expression was negatively regulated by AGTPBP1. Mechanistically, AGTPBP1-mediated repression of EVPL led to the activation of the ERK signaling pathway, as evidenced by increased phosphorylation of ERK1/2. Rescue experiments confirmed that EVPL overexpression attenuated AGTPBP1-induced malignant phenotypes and ERK activation. CONCLUSION: This study unveils a novel oncogenic role of AGTPBP1 in breast cancer. We delineate a previously unrecognized AGTPBP1/EVPL/ERK axis whereby AGTPBP1 drives tumor progression by simultaneously disrupting intercellular adhesion and activating pro-tumorigenic ERK signaling. Our findings propose AGTPBP1 as a potential therapeutic target for breast cancer intervention.
Serum-free medium modulates the immunomodulatory and anabolic function of equine bone marrow-derived mesenchymal stromal cells.
Tehrani AH, Toth K, Osinchuk N … +4 more , Dufour A, Krawetz R, Sen A, Sparks H
Exp Cell Res · 2026 Jun · PMID 41895434 · Publisher ↗
Adult bone marrow-derived mesenchymal stromal cells (BM-MSCs) hold significant therapeutic potential in human and veterinary medicine. Traditionally, BM-MSC cultures use fetal bovine serum (FBS) to promote growth, but th...
Adult bone marrow-derived mesenchymal stromal cells (BM-MSCs) hold significant therapeutic potential in human and veterinary medicine. Traditionally, BM-MSC cultures use fetal bovine serum (FBS) to promote growth, but this practice introduces batch variability and xenogeneic contamination that complicate clinical translation. While serum-free medium (SFM) alternatives have been optimized for human MSCs, limited options have been explored for alternative or veterinary species. Here, we compared a chemically defined, customizable SFM formulation with conventional serum-containing medium (SCM) for isolation and expansion of equine bone marrow mesenchymal cells (eqBM-MSCs). Both conditions supported adherence and trilineage differentiation. However, SFM cultures maintained a colony-based growth pattern across passages and showed up to 3-fold higher colony-forming output. SFM cells were enriched for a CD29 population relative to SCM, despite slower proliferation. At early passage, SFM cells displayed a two-fold longer population doubling time than SCM with reduced cumulative expansion across serial passaging. Quantitative proteomics indicated that SFM expansion was associated with increased abundance of proteins mapping to immune signaling and repair-related pathways, including neutrophil degranulation, interferon-associated signaling, and hemostasis/angiogenesis, whereas SCM was enriched for pathways linked to proliferation and metabolism. Cytokine profiling further showed elevated KC-GRO, IL-8, and FGF in SFM relative to SCM. Together, these findings demonstrate the potential of a defined SFM platform to modulate eqBM-MSC growth behavior and protein/cytokine signatures, while highlighting a scalability trade-off between yield and phenotype that will require further optimization and functional validation.
Research topics and trends of pyroptosis based on bibliometric analysis.
Leng Q, Sun X, Wang P
Exp Cell Res · 2026 May · PMID 41887451 · Publisher ↗
This study employs bibliometric methods, utilizing tools such as CiteSpace and VOSviewer, to conduct a multidimensional analysis of literatures on cell pyroptosis indexed in the Web of Science Core Collection. The resear...
This study employs bibliometric methods, utilizing tools such as CiteSpace and VOSviewer, to conduct a multidimensional analysis of literatures on cell pyroptosis indexed in the Web of Science Core Collection. The research encompasses global publication trends, national collaboration networks, institutional competitiveness, keyword trends, and citation clustering, aiming to reveal the knowledge landscape and frontiers of this field. Current studies in pyroptosis highlight a global collaborative framework centered on China and the US. This has led to the emergence of two highly effective institutional research modes: one that maintains an equilibrium between volume and impact, and another that prioritizes top-tier elite quality. This study reveals that the field has evolved from investigating the fundamental mechanisms of inflammasomes (such as NLRP3 assembly) to discovering effector protein functions (centered on GSDMD), and subsequently to elucidating pathological mechanisms and exploring clinical applications. By ranking keywords based on integrated metrics and trend factor analysis, this study identifies three major frontier directions: (1) Deepening mechanistic research, shifting from classical pathways to complex regulatory networks involving cellular metabolic homeostasis and pyroptosis; (2) Establishing new frameworks for programmed cell death mode interactions, exemplified by PANoptosis; (3) Focusing on GSDM protein-targeted therapies and nanodelivery technology development to advance clinical translation.
The antineoplastic agent streptozotocin induces short-term telomere instability in Epstein-Barr virus-transformed human lymphoblastoid cells.
Cardozo AG, Castrogiovanni DC, Parisi J … +1 more , Bolzán AD
Exp Cell Res · 2026 Jun · PMID 41887450 · Publisher ↗
We assessed the induction of telomere instability-related chromosomal aberrations by streptozotocin (STZ) in human lymphoblastoid cells (T-37) immortalized with Epstein-Barr virus (EBV) using Peptide Nucleic Acid-Fluores...
We assessed the induction of telomere instability-related chromosomal aberrations by streptozotocin (STZ) in human lymphoblastoid cells (T-37) immortalized with Epstein-Barr virus (EBV) using Peptide Nucleic Acid-Fluorescence In Situ Hibridization (PNA-FISH) with pan-telomeric and pan-centromeric probes. Cells were exposed to STZ at concentrations ranging from 0.5 to 4.0 mM in sodium citrate (SC, pH 4.4) for 1 h at 37 °C, and chromosomal aberrations were analyzed 24 h later. Incomplete chromosome elements (ICE) significantly increased after STZ treatments at 2 and 4 mM compared to untreated and SC-treated cultures (p < 0.05). The total number of telomeric signals lost (TSL) and the frequency of chromosome-type telomere signal loss per cell rose significantly after STZ treatments of 0.5 and 1 mM compared to untreated and SC-treated cultures (p < 0.05). Both SC and STZ caused chromatid-type telomere signal loss and duplications (TSD), but differences between these treatments were non-significant (p > 0.05). Non-significant differences between treatments in terms of telomere fusions, associations, ectopic signals, or sister-chromatid telomere fusions were observed (p > 0.05). Quantitative FISH (Q-FISH) revealed longer telomeres in cells treated with SC (10 and 60 μL) or STZ (0.5, 1, and 3 mM) compared to untreated cells (p < 0.05), with non-significant differences between SC and STZ (p > 0.05). These results indicate that STZ induces short-term telomere instability, while suggest that SC induces telomere dysfunction and elongation in human lymphoblastoid cells.
Metabolic cell biology - Do. Or do not. There is no try.
Liu JL
Exp Cell Res · 2026 Jun · PMID 41871731 · Publisher ↗
Abstract loading — click title to view on PubMed.
ZFP36 and CEBPA are macrophage-associated prognostic biomarkers linked to glomerular endothelial inflammation in ANCA-associated glomerulonephritis.
Ni A, Zhu X, Wang J … +8 more , Chen L, Zhu H, Miao J, Xu J, Ren P, Chen J, Xiao L, Han F
Exp Cell Res · 2026 May · PMID 41865826 · Publisher ↗
BACKGROUND: Macrophages are critical in antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (AAGN). This study investigated macrophage-associated genes (MAGs) ZFP36 and CEBPA in AAGN renal tissue and...
BACKGROUND: Macrophages are critical in antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (AAGN). This study investigated macrophage-associated genes (MAGs) ZFP36 and CEBPA in AAGN renal tissue and evaluated their role in glomerular endothelial injury. METHODS: Macrophage infiltration and its association with prognosis were assessed in renal tissues via immunohistochemistry. ZFP36 and CEBPA were identified via the Gene Expression Omnibus (GEO) database. Their expression in AAGN and correlation with immune cell infiltration and clinical indicators were analyzed. Serum from healthy individuals and AAGN patients was used to stimulate human renal glomerular endothelial cells (HRGECs), and ZFP36 and CEBPA expression was measured using western blotting and real-time PCR. Functional studies included gene knockdown and overexpression, actinomycin D chase assays, NF-κB inhibition, and a direct co-culture system with THP-1-derived macrophages. RESULTS: AAGN renal tissues showed marked immune infiltration and macrophage activation, predicting poor prognosis. ZFP36 was downregulated and low ZFP36 expression correlated with poor prognosis, while CEBPA was upregulated and high CEBPA expression correlated with poor prognosis. Immunofluorescence demonstrated partial localization of both proteins in CD31-positive glomerular endothelial areas. In HRGECs, ZFP36 attenuated inflammatory responses, accelerated TNF-α and IL6 mRNA decay, and was associated with reduced NF-κB activation, whereas CEBPA promoted endothelial inflammatory mediator expression. In co-culture experiments, endothelial ZFP36 reduced, whereas endothelial CEBPA increased, TNF-α production in adjacent macrophages. CONCLUSIONS: ZFP36 and CEBPA are macrophage-associated genes linked to immune infiltration, renal prognosis, and endothelial inflammatory responses in AAGN, and may serve as potential tissue biomarkers and therapeutic targets.
Age-dependent decline in plasmalogen biosynthesis impairs stress-induced mitochondrial fission in Drosophila.
Kumar A, Das A, Stewart T … +3 more , Hsu FF, Kang P, Bai H
Exp Cell Res · 2026 May · PMID 41865825 · Full text
Mitochondrial dynamics, maintained by balanced fission and fusion, are essential for organelle quality control and cellular homeostasis, yet this process becomes disrupted during aging. The upstream cues underlying age-a...
Mitochondrial dynamics, maintained by balanced fission and fusion, are essential for organelle quality control and cellular homeostasis, yet this process becomes disrupted during aging. The upstream cues underlying age-associated fission defects remain poorly defined. Here, using Drosophila oenocytes (hepatocyte-like cells), we show that aging drives progressive mitochondrial enlargement and morphological abnormalities. Live-cell imaging analysis demonstrated that young oenocytes rapidly undergo mitochondrial fission in response to paraquat-induced oxidative stress, whereas aged oenocytes fail to fragment, resulting in persistently enlarged mitochondria. This age-dependent fission defect correlates with a marked decline in mitochondrial plasmalogen levels, a class of ether phospholipids enriched in mitochondrial membranes. In addition, genetic disruption of plasmalogen biosynthesis using a hypomorphic mutation in the plasmanylethanolamine desaturase Kua (TMEM189) recapitulated the aging phenotype. These findings establish that an age-dependent decline in plasmalogen biosynthesis impairs mitochondrial fission, leading to persistent mitochondrial enlargement. Thus, loss of plasmalogen-dependent membrane dynamics represents a novel mechanism driving mitochondrial dysfunction during aging in metabolic tissues.
AURKA promotes radioresistance in pancreatic cancer via GSK3β-mediated PTEN phosphorylation at T366.
Chen D, Zhu X, Tong J … +6 more , Huang C, Chen W, Xu B, Chen L, Ye C, Zhang H
Exp Cell Res · 2026 May · PMID 41864259 · Publisher ↗
Radioresistance is a major therapeutic challenge in clinical management of pancreatic ductal adenocarcinoma (PDAC), yet the molecular mechanisms governing this process remain largely elusive. In this study, it was demons...
Radioresistance is a major therapeutic challenge in clinical management of pancreatic ductal adenocarcinoma (PDAC), yet the molecular mechanisms governing this process remain largely elusive. In this study, it was demonstrated that the oncogenic kinase Aurora Kinase A (AURKA) drove radioresistance by orchestrating a signaling cascade that inhibited the tumor suppressor PTEN. Analysis of patient cohorts and TCGA data revealed that AURKA was overexpressed in PDAC, and its expression levels were found to robustly correlate with poor patient prognosis. Functionally, AURKA overexpression conferred potent radioresistance, yielding SER values of 0.847 ± 0.086 and 0.824 ± 0.073 in PANC-1 and SW1990 cells, respectively. AURKA overexpression not only markedly enhanced cellular proliferation and migration but also significantly suppressed apoptosis. Mechanistically, Co-IP uncovered that AURKA physically interacted with Glycogen Synthase Kinase 3β (GSK3β). This interaction facilitated the inhibitory phosphorylation of the tumor suppressor PTEN at Threonine 366, which impaired PTEN's phosphatase activity and led to sustained activation of the pro-survival PI3K/AKT/mTOR pathway. Critically, this radioresistant phenotype was reversed by either GSK3β knockdown or the expression of a phosphorylation-deficient PTEN-T366A mutant, confirming the essentiality of this signaling axis. Collectively, this study discovered a novel and clinically relevant AURKA-GSK3β-PTEN signaling axis that mechanistically linked AURKA overexpression to radioresistance in PDAC. Furthermore, our findings provide a strong mechanistic rationale for targeting AURKA, revealing a promising therapeutic strategy to overcome radioresistance and improve therapeutic outcomes in pancreatic cancer.
The cGAS-STING signaling pathway mediates pyroptosis in colonic epithelial cells and accelerates the progression of CAC.
Wang J, Luo A, Yao Y … +2 more , Liu A, Zhu X
Exp Cell Res · 2026 May · PMID 41864258 · Publisher ↗
OBJECTIVE: Colitis-associated cancer (CAC) is a minor subtype of CRC, accounting for 2% of CRC cases. It is also one of the most common and severe complications in patients with chronic IBD. The exact pathogenic mechanis...
OBJECTIVE: Colitis-associated cancer (CAC) is a minor subtype of CRC, accounting for 2% of CRC cases. It is also one of the most common and severe complications in patients with chronic IBD. The exact pathogenic mechanisms of CAC remain unclear. Therefore, actively investigating the pathogenesis of CAC and developing novel therapeutic strategies are of great significance for its prevention and treatment. METHODS: The mouse model of UC and CAC was induced using DSS and AOM stimulation. The model was validated through H&E staining, Masson, AB-PAS staining, and ELISA assays. Additionally, the expression levels of key molecules, including cGAS and STING, were examined in model mice using qRT-PCR and immunohistochemistry. Later, based on the mouse CAC model, STING inhibitors and agonists were administered in combination with H&E staining, Masson, AB-PAS staining, and ELISA assays to explore the impact of key molecular expression levels on CAC progression in mice. Finally, in a mouse UC organoid model, STING agonists were used in combination with NLRP3 inhibitor. WB, CCK8, immunofluorescence staining, and intestinal permeability tests were employed to investigate the regulatory mechanisms of pyroptosis in CAC development. RESULTS: DSS and AOM stimulation successfully induced the mouse UC and CAC model. Key proteins of the cGAS-STING pathway, including cGAS, p65, and IFN-I, were significantly upregulated in the mouse UC and CAC model. The STING agonist SR-717 markedly increased the expression of cGAS-STING pathway-related genes, such as cGAS, STING, p65, and IFN-I, exacerbating pathological features and serum inflammatory cytokine levels in the colonic cancer model. It also significantly upregulated pyroptosis marker proteins pro-caspase-1, GSDMD-N, and NLRP3, whereas the STING inhibitor H-151 effectively suppressed these effects. The NLRP3 inhibitor INF195 enhanced the proliferative capacity, membrane integrity, and intestinal barrier function of the mouse colon organoid model, providing partial protective effects. Meanwhile, the STING agonist SR-717 partially reversed the effects of INF195. CONCLUSION: The cGAS-STING signaling pathway accelerates the progression of CAC by promoting pyroptosis in colonic epithelial cells through NLRP3/caspase-1 mediation.
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