Molecular medicine reports最新文献

{"title":"Intestinal CD4⁺ T cells treated with <i>Pseudostellaria heterophylla</i> polysaccharide improve insulin resistance in BNL CL.2 cells by modulating PI3K/AKT signaling and energy metabolism.","authors":"Yongjun Kan, Yingying Liu, Yating Huang, Li Zhao, Jiang Chang, Wensheng Pang, Wenxiong Lin, Juan Hu","doi":"10.3892/mmr.2025.13682","DOIUrl":"10.3892/mmr.2025.13682","url":null,"abstract":"<p><p><i>Pseudostellaria heterophylla</i> polysaccharide PF40 has shown potential in alleviating insulin resistance by modulating CD4⁺ T cells in the intestinal tissue of rats with type 2 diabetes mellitus. To further elucidate the underlying mechanism, CD4⁺ T cells were isolated from the intestinal tissue of rats treated with PF40 (P‑T) and co‑cultured with insulin‑resistant (IR)‑BNL CL.2 cells. Oxidative stress was assessed by measuring reactive oxygen species, malondialdehyde and superoxide dismutase activity, while apoptosis was evaluated by flow cytometry. Insulin sensitivity was examined by glucose uptake and consumption assays. Protein expression related to the PI3K/AKT pathway was determined by western blotting, and targeted energy metabolomics was performed to analyze glycolysis and the tricarboxylic acid cycle. P‑T treatment reduced oxidative stress in IR‑BNL CL.2 cells by reducing reactive oxygen species and malondialdehyde levels, while increasing superoxide dismutase activity. Additionally, P‑T inhibited apoptosis and improved insulin sensitivity, as evidenced by the increased glucose uptake and consumption. Mechanistically, P‑T decreased phosphorylated‑insulin receptor substrate‑1 expression, leading to activation of the PI3K/AKT signaling pathway, which enhanced glucose metabolism. Targeted energy metabolomics analysis further revealed that P‑T regulated glycolysis and the tricarboxylic acid cycle, ameliorating energy metabolism dysfunction. Notably, the combined treatment of PF40 and metformin indicated potential synergistic effects. These findings highlight the critical role of intestinal CD4⁺ T cells in PF40‑mediated metabolic regulation, suggesting that targeted modulation of intestinal immune cell homeostasis may offer a promising strategy for the prevention and treatment of insulin resistance.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Capsaicin attenuates sepsis‑associated encephalopathy by inhibiting neuroinflammation and apoptosis whilst activating mitophagy through the BNIP3/NIX pathway.","authors":"Silun Zhang, Nanbo Luo, Hanxi Wu, Junfa Chen, Yonghan Jiang, Lifei Xiao, Hanlin Liang, Qingsheng Xue, Yan Luo, Buwei Yu, Yuqiang Liu, Zhiheng Liu","doi":"10.3892/mmr.2025.13686","DOIUrl":"10.3892/mmr.2025.13686","url":null,"abstract":"<p><p>Sepsis‑induced abnormalities in brain function or sepsis‑associated encephalopathy (SAE) can manifest as cognitive dysfunction and other neuropsychiatric symptoms; however, the underlying mechanisms remain unclear. The aim of the present study was to elucidate the possible effects and mechanism of capsaicin, a transient receptor potential vanilloid 1 (TRPV1) agonist, on the pathological features of SAE. A model of SAE in C57BL/6 mice was generated using cecal ligation and puncture (CLP). Capsaicin (1 mg/kg) was injected subcutaneously before surgery. Cognitive function in mice was evaluated using the novel object recognition test (NORT) and Morris water maze (MWM). Immunofluorescence staining, ELISA, western blotting and transmission electron microscopy were performed to detect the degree of microglial activation (ionized calcium‑binding adapter molecule 1), proinflammatory cytokine levels (TNF‑α), autophagy and apoptosis‑related protein expression, and autophagosomes. Autophagic flux was monitored using the LC3‑GFP‑mCherry fluorescent reporter. Compared with that in the sham group mice, the expression levels of TRPV1 were significantly reduced in the hippocampal tissue of mice with sepsis. Mice with sepsis also exhibited cognitive dysfunction. Notably, a single administration of capsaicin reduced the mortality rate, but did not improve cognitive function in mice with sepsis. Furthermore, repeated administration of capsaicin was revealed to enhance the recognition index of novel objects among mice with sepsis, to reduce the latency to locate the platform and to augment the duration of mouse platform quadrant movements, according to the NORT and MWM tasks. Increased microglial activation, release of proinflammatory cytokines and expression levels of apoptosis‑related proteins were all observed in mice with CLP‑induced sepsis, as was brain tissue destruction in the hippocampal regions. By contrast, capsaicin treatment ameliorated CLP‑induced microglial activation, inflammation, neuronal apoptosis (cleaved caspase 3 expression increased) and brain tissue destruction. Furthermore, application of capsaicin increased the expression levels of LC3, reduced the expression of p62 and elevated autophagic flux compared with those in the CLP group. Finally, treatment with capsaicin effectively enhanced the levels of Bcl‑2‑interacting protein 3 (BNIP3) and BNIP3‑like (NIX) expression. These findings suggested that capsaicin may be considered a potential drug for the treatment of SAE, and BNIP3/NIX‑mediated mitophagy may be involved in this process.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12461237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] PirB restricts neuronal regeneration in developing rat brain following hypoxia‑ischemia.","authors":"Hua Wang, Ying Xiong, Dezhi Mu","doi":"10.3892/mmr.2025.13688","DOIUrl":"10.3892/mmr.2025.13688","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the immunofluorescence images shown in Fig. 3, the 'HIBD' panel appeared to share an overlapping section of data with the adjoining 'HIBD+anti PirB' panel, albeit the data held in common appeared to have been vertically stretched in the latter panel. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 6: 339‑344, 2012; DOI: 10.3892/mmr.2012.907].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGFβ1‑induced epithelial‑mesenchymal transition is associated with stathmin downregulation and increased microtubule stability in bronchial epithelial cells.","authors":"Nur Amilia Hanie Mohamad Hasan, Yu Zhao Lee, Chau Ling Tham, Daud Ahmad Israf, Nuzul Noorahya Jambari, Hanis Hazeera Harith","doi":"10.3892/mmr.2025.13684","DOIUrl":"https://doi.org/10.3892/mmr.2025.13684","url":null,"abstract":"<p><p>Epithelial‑mesenchymal transition (EMT) is a pathophysiological process contributing to bronchial remodeling in airway diseases such as chronic obstructive pulmonary disorder. EMT in several types of cancer involves dysregulated microtubule dynamics. Stathmin, a microtubule destabilizer, is highly expressed in different types of cancer, and is associated with decreased microtubule stability and enhanced migratory capability. The present study examined the relationship between stathmin expression and microtubule stability in bronchial EMT using an <i>in vitro</i> model. Primary normal human bronchial epithelial (NHBE) cells and the BEAS‑2B bronchial epithelial cell line were induced with TGFβ1 for 48 or 72 h to activate EMT, with or without the TGFβ1 inhibitor, SB431542. TGFβ1‑induced cells exhibited significantly reduced E‑cadherin (epithelial marker) and increased vimentin (mesenchymal marker) expression, which was inhibited by SB431542. TGFβ1‑mediated EMT was associated with reduced stathmin levels and increased microtubule stability (indicated by acetylated‑α‑tubulin) in BEAS‑2B and NHBE cells. However, TGFβ1‑induced EMT did not significantly enhance cell migration, potentially due to stabilized microtubules. By contrast, 10% fetal bovine serum induced a more robust EMT phenotype, accompanied by increased stathmin expression, reduced microtubule stability and enhanced cell migration. The present study highlights the potential role of stathmin in modulating microtubule dynamics during bronchial remodeling and hypothesizes its involvement in the transition from partial to full EMT, depending on the EMT‑inducing stimulus.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of CXCL8 by endoplasmic reticulum stress promotes migration and invasion of esophageal squamous cell carcinoma through activation of SMAD2/3.","authors":"Junhong Wu, Fangyu Su, Juntao Lu, Huanchen Xu, Xia Yang, Fei Li, Lei Liu, Wei Guo","doi":"10.3892/mmr.2025.13676","DOIUrl":"10.3892/mmr.2025.13676","url":null,"abstract":"<p><p>Endoplasmic reticulum stress (ERS) is a protective stress response aimed at mitigating its own abnormal proteins, which is closely associated with tumors. However, the molecular mechanism of ERS in the pathogenesis of esophageal squamous cell carcinoma (ESCC) remains unclear. In the present study, RNA sequencing was carried out in the ESCC ERS cell model <i>in vitro</i>, and differentially expressed genes were screened, among which CXCL8 with exhibited differential expression which was studied. CXCL8 was significantly upregulated after thapsigargin (TG; an ERS inducer) treatment in ESCC cells. A marked elevated expression of CXCL8 and its receptors were observed in ESCC cells. CXCL8 was induced by the IRE1α and PERK pathways of ERS, transcription of which was activated by the downstream transcription factors XBP1 and ATF4. TG and rh‑CXCL8 facilitated migration and invasion of ESCC cells, and the migration and invasion effect of TG on ESCC cells could be partially prevented by knockdown of CXCR1. Furthermore, CXCL8‑CXCR1 could activate SMAD2/3 and the activation of SMAD2/3 directly or indirectly regulated the transcription of SNAI2 and ZEB1 to promote the progression of epithelial‑mesenchymal transition (EMT) in ESCC. Both <i>in vivo</i> experiments and immunohistochemical analyses further demonstrated the oncogenic effects of CXCL8. In conclusion, the data obtained in the present study indicated that CXCL8 may be induced via the IRE1α/XBP1 and PERK/ATF4 pathways, and that the CXCL8‑CXCR1/2‑SMAD2/3‑SNAI2/ZEB1 axis is involved in the EMT process of ER‑stressed ESCC cells. Thus, blocking the CXCL8‑CXCR1/2 axis may disrupt ERS‑induced migration and invasion of ESCC cells, thereby improving the prognosis of patients with ESCC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 5","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] MicroRNA‑363‑3p is downregulated in hepatocellular carcinoma and inhibits tumorigenesis by directly targeting specificity protein 1.","authors":"Jie Ying, Xuechun Yu, Chaojian Ma, Yongqi Zhang, Jingwu Dong","doi":"10.3892/mmr.2025.13699","DOIUrl":"https://doi.org/10.3892/mmr.2025.13699","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a reader that, regarding the Transwell assay data shown in Fig 5, there was a slight concern that the data panels showing the results for the migration and invasion assay experiments for the two investigated cell lines (Hep3B and SMMC‑7721) may have respectively originated from the same photos. Moreover, the 'Hep3B/Migration/miR‑363‑3p mimics + pcDNA3.1‑Sp1' and SMMC‑67721/Invasion/miR‑363‑3p mimics + pcDNA3.1‑Sp1' data panels contained an area of overlapping data, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source. A subsequent analysis of the data in this paper revealed that there were a number of internal data duplications comparing Figs. 2C and 5 in this paper, and certain of these data had already been submitted for publication in an article written by different authors at different research institutes to the journal Oncology Letters. In view of the fact that the abovementioned data had already been submitted for publication before this paper was submitted to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply.. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 1603‑1611, 2017; DOI: 10.3892/mmr.2017.6759].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory role of POSTN in keloid pathogenesis.","authors":"Bin Jiang, Fan Zhuo, Xiahong Li, Kaoyuan Zhang, Jiaxu Gu, Jingwen Wu, Weilong Zhong, Yanfen Zou, Bo Yu, Cong Huang","doi":"10.3892/mmr.2025.13701","DOIUrl":"https://doi.org/10.3892/mmr.2025.13701","url":null,"abstract":"<p><p>Keloids are an inflammatory cutaneous condition, which are characterized by fibroproliferative overgrowth of the skin. Although keloids are not life‑threatening, their incidence and recurrence are relatively high, thus decreasing the quality of life of patients due to pain, pruritus and cosmetic reasons. Additionally, the precise molecular mechanisms underlying the pathogenesis of keloids remain largely unexplored, thus limiting the development of therapeutic interventions. To screen the key molecules in keloids, microarray data were selected from three different datasets obtained from the Gene Expression Omnibus database, namely GSE145725, GSE7890 and GSE44270. One differentially expressed gene was identified, periostin (POSTN), which was upregulated in keloid fibroblasts (KFs) compared with normal fibroblasts. Its high expression was further validated in KFs using reverse transcription‑quantitative PCR (RT‑qPCR), western blotting and immunofluorescence staining. Its potential function were explored in keloids through loss-of-function assay. Notably, the EdU incorporation assay and cell cycle assay indicated that POSTN knockdown had limited effects on the proliferation of KFs; however, the RT‑qPCR, western blotting, and RNA sequencing results suggested that POSTN inhibition blocked the JAK‑STAT signaling pathway and decreased the expression levels of various proinflammatory factors in KFs. Additionally, the RT‑qPCR and western blotting results demonstrated that IL‑4 and IL‑13, two significant mediators of T helper 2 (Th2) signaling, could induce POSTN expression in KFs. Notably, IL‑4 receptor (IL‑4R), a receptor for both IL‑4 and IL‑13, could be positively modulated by POSTN through the Reactome enrichment, RT‑qPCR and western blotting analysis. Furthermore, IL‑4R was essential for IL‑4/IL‑13‑induced POSTN upregulation in KFs, thus indicating a positive feedback loop between POSTN and Th2 signaling. Overall, the current study uncovered a novel mechanism of POSTN, which could be associated with keloid inflammation, thus highlighting the POSTN/Th2 feedback loop as a potential therapeutic target for patients with keloids.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the gut‑lung axis in bronchopulmonary dysplasia: Physiological basis, pathogenesis and immunological modulation (Review).","authors":"Yue Zhu, Rui-Dong Ding","doi":"10.3892/mmr.2025.13678","DOIUrl":"10.3892/mmr.2025.13678","url":null,"abstract":"<p><p>Bronchopulmonary dysplasia (BPD) is a severe respiratory condition that affects preterm infants, which is frequently associated with a poor long‑term prognosis. The gut‑lung axis is a bidirectional communication pathway mediated by microbial communities and shared immune mechanisms that has emerged as a important area of research. It has been indicated that gut microbiota can influence the progression of various pulmonary diseases, where the gut‑lung axis can affect the progression of BPD through various mechanisms, such as bacterial translocation, microbial metabolite exchange, inflammatory cytokine spillover and immune cell migration. Although the relationship between the gut‑lung axis and BPD remains under exploration, understanding this interaction may identify early warning markers and novel therapeutic strategies for BPD. The present review summarizes the influence of the gut‑lung axis on BPD, focusing on the bidirectional communication and gut microenvironmental changes during BPD and the possible immunoregulatory mechanisms involved. By elucidating these associations, the present review aims to provide novel insights into the prevention and treatment of BPD.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145041005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated metabolomics and transcriptomics analyses reveal changes in metabolites and their associated gene expression in the blood of patients with recurrent HSV‑2 genital herpes.","authors":"Jianping He, Chenxi Feng, Yaohan Xu, Yan Chen, Siji Chen, Jiang Zhu, Yinjing Song, Hao Cheng","doi":"10.3892/mmr.2025.13681","DOIUrl":"10.3892/mmr.2025.13681","url":null,"abstract":"<p><p>Genital herpes (GH), which is primarily caused by herpes simplex virus type 2 (HSV‑2), is the leading cause of genital ulcers worldwide, and is characterized by recurring outbreaks of painful genital lesions. Despite the high prevalence of GH, the metabolic and transcriptomic mechanisms underlying disease recurrence remain poorly understood. Therefore, the present study aimed to identify metabolic alterations in patients with HSV‑2 GH via integrating transcriptomics, metabolomics and single‑cell RNA‑sequencing (scRNA‑seq) analyses. Non‑targeted metabolomics identified significant changes in pathways associated with glycerophospholipid metabolism, amino acid biosynthesis and cholesterol metabolism. In addition, RNA‑seq analysis revealed that genes associated with the alanine, aspartate and glutamate, and valine, leucine and isoleucine metabolism pathways were significantly upregulated in patients with recurrent HSV‑2 GH. Furthermore, scRNA‑seq data showed that <i>IDH1</i> and <i>ETNK1</i> were upregulated, mainly in dendritic cells (DCs), plasmacytoid DCs and monocytes derived from patients with GH. Notably, the expression levels of genes associated with oxidative phosphorylation, such as <i>MT‑CYB</i> and <i>MT‑CO3</i>, were significantly elevated across monocytes, T cells and B cells. Overall, the results of the current study suggested that metabolic reprogramming could occur in patients with recurrent HSV‑2 GH, thus providing potential biomarkers and therapeutic targets that could be involved in the future development of treatment approaches.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory effect of antibodies against the cell adhesion molecule gicerin on gastric cancer progression.","authors":"Saaya Ueno, Nao Uemura, Kazuhide Adachi, Yasuhiro Tsukamoto","doi":"10.3892/mmr.2025.13687","DOIUrl":"10.3892/mmr.2025.13687","url":null,"abstract":"<p><p>Gicerin is a member of the immunoglobulin superfamily, which functions as a cell adhesion molecule that is expressed in developing and regenerating tissues, as well as in various types of tumors. In malignant neoplasms, gicerin has been implicated in promoting cellular invasion and metastasis. The present study aimed to investigate whether or not anti‑gicerin antibodies could inhibit the progression of the human gastric cancer cell line NUGC‑4 in a murine model. First, immunofluorescence staining was employed to confirm gicerin expression in the NUGC‑4 cells. The cells were subsequently pretreated with either anti‑gicerin antibodies or pre‑immune IgG and transplanted subcutaneously into nude mice, where the extent of tumor growth and local invasion were both assessed. In a separate hematogenous metastasis model, mice received a tail‑vein injection of NUGC‑4 cells pretreated in an identical manner and pulmonary metastases were evaluated. Anti‑gicerin antibody pretreatment led to a significant suppression of subcutaneous tumor formation, histological invasiveness and lung nodule formation compared with the controls. Taken together, these findings suggested that the antibody‑mediated inhibition of gicerin reduced both local tumor progression and hematogenous spread in gastric cancer, highlighting gicerin as a promising therapeutic target that potentially may be effective when used in combination with conventional chemotherapy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12461236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}