Molecular and Cellular Probes最新文献

{"title":"Copy number variations in urine cell-free DNA from bladder neoplasm patients","authors":"Cuello Garcia Haider ,&nbsp;Qichao Wang ,&nbsp;Guangyue Wang ,&nbsp;Yinfeng Wang ,&nbsp;Yutong Fu ,&nbsp;Zhoufan Zhang ,&nbsp;Changling Cao ,&nbsp;Fengcheng Xue ,&nbsp;Haitao Liu ,&nbsp;Qian Wang ,&nbsp;Jie Zhou ,&nbsp;Tingya Jiang ,&nbsp;Jingyi Cao ,&nbsp;Yang Zhou","doi":"10.1016/j.mcp.2025.102044","DOIUrl":"10.1016/j.mcp.2025.102044","url":null,"abstract":"<div><div>Bladder cancer is a common malignancy, and its diagnosis is based on invasive procedures such as cystoscopy. Genetic aberrations play an important role in the development of many diseases, including bladder cancer. As a result, identifying the genetic basis of a disease can provide useful information for early diagnosis and therapy. Cell-free DNA (cfDNA) offers a non-invasive approach to extract genetic information, which could be valuable for establishing the genetic cause of bladder cancer. In this study, we analyzed copy number variations (CNV) in urine cfDNA from 20 patients, with cystoscopy confirmed bladder cancer, sequenced by next-generation sequencing (NGS) and their CNV examined using the whole genome sequence. Statistical analysis of the carcinoma samples included Wilcoxon and Chi-square tests (p ≤ 0.005). Different patterns in CNV were identified in Chromosomes 1, 2, 3, 5, 6, 8, 9, 10, 11, 12, 17, 19, and 20 with the chromosome cytobands showing significant difference in variation patterns in patient parameters, such as smoking habit, number of tumors, grade of the tumors, and invasiveness. The genes that exhibited distinct CNV in each chromosomal cytoband have been associated with the development and progression of various cancers including bladder cancer indicating the clinical significance of CNVs as a useful tool for disease diagnosis. Therefore, this study demonstrates that by using NGS, CNV in urine cfDNA can provide valuable information on the state of blader cancer which can be further utilized to investigate therapies or early diagnosis.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"83 ","pages":"Article 102044"},"PeriodicalIF":2.3,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144676347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ubiquitin-specific peptidase 53 suppresses the tumorigenesis of breast cancer cells and its related gene analysis","authors":"Hongbo Lan ,&nbsp;Lina Peng ,&nbsp;Fei Chen ,&nbsp;Kun Xie ,&nbsp;Futing Mu ,&nbsp;Jingshuang Wang ,&nbsp;Juanjuan Mei ,&nbsp;Wenhui Yan","doi":"10.1016/j.mcp.2025.102043","DOIUrl":"10.1016/j.mcp.2025.102043","url":null,"abstract":"<div><h3>Background</h3><div>Breast cancer (BC) remains the most common malignancy affecting women's health globally. Thus, elucidating the molecular mechanisms driving BC progression and identifying novel therapeutic targets is imperative. Ubiquitin-specific peptidase 53 (USP53) is a deubiquitinating enzyme reported to exert tumor-suppressive effects in several types of cancers. However, USP53 has been poorly studied in BC.</div></div><div><h3>Methods</h3><div>Based on the TCGA database and GTEx transcriptome data, differentially expressed genes in BC were screened, and the relationship between USP53 expression and BC characteristics and prognosis were analyzed. qRT-PCR, Western blot, and immunohistochemistry determined USP53 expression. After transfection, BC cells’ proliferation, migration, and invasion were assessed using CCK-8 and Transwell assay. A subcutaneous xenograft tumor model in nude mice was used to evaluate the <em>in vivo</em> effect of USP53. Besides, USP53 expression-associated immune cells were screened using the Cibersort package.</div></div><div><h3>Results</h3><div>USP53 expression was reduced in BC patients and showed potential diagnostic significance. Functionally, overexpressing USP53 inhibited BC cell proliferation, migration, and invasion, while silencing it promoted these malignant behaviors. <em>In vivo</em>, tumors derived from USP53-overexpressing cells grew more slowly and exhibited lower Ki67 expression. Additionally, we found that Tcm, T helper cells, Mast cells, and Eosinophils were positively associated with USP53 expression, whereas NK CD56dim cells and TReg were negatively associated with USP53 expression.</div></div><div><h3>Conclusions</h3><div>Together, we proved that USP53 was down-regulated in BC and weakened the malignant progression of BC cells both <em>in vitro</em> and <em>in vivo</em>. USP53 was also associated with a variety of immune cells. Our study suggested that USP53 may be a novel target for BC therapy.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"83 ","pages":"Article 102043"},"PeriodicalIF":2.3,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RCN1 affects malignant progression and macrophage M2 polarization in diffuse large B-cell lymphoma","authors":"Qiuyu Zhu ,&nbsp;Xiafang Yang","doi":"10.1016/j.mcp.2025.102042","DOIUrl":"10.1016/j.mcp.2025.102042","url":null,"abstract":"<div><div>Malignant behaviors of cancer cells and immune evasion by macrophage can lead to treatment failure in diffuse large B-cell lymphoma (DLBCL). Recent studies have revealed the aberrant expression of reticulocalbin 1 (RCN1) that is associated with malignant progression of several cancers. Nevertheless, its roles in DLBCL remain unclear. In this present study, several online bioinformatics databases substantiated high expression of RCN1 in tumor samples from DLBCL patients. Furthermore, there were obvious elevation of RCN1in tumor specimens form our collected tissues and DLBCL cells. Importantly, the shorter survival outcome was observed in patients with high levels of RCN1. Intriguingly, down-regulation of RCN1 attenuated DLBCL cell viability, invasion ability and increased cancer cell apoptosis. Moreover, TIMER database revealed the correlation between RCN1 expression and tumor-infiltrating macrophages, and M2 macrophage markers in DLBCL patients. Knockdown of RCN1 suppressed cancer cell ability to induce macrophage M2-like polarization by inhibiting the percentage of CD163⁺ macrophages and expression of M2-like markers (CD163, CD204, and IL-10). Concomitantly, M2 macrophage-induced cancer cell viability and invasion was abrogated after RCN1 down-regulation. Further assay revealed that knockdown of RCN1 suppressed activation of the PI3K/AKT signaling in DLBCL cells. Notably, reactivation this pathway via its agonist 740Y-P offset the anti-tumor efficacy of RCN1 knockdown in cancer cell malignancy and macrophage polarization towards M2 phenotype. Therefore, RCN1 may contribute to the malignant progression of DLBCL by directly regulating cancer cell behavior and indirectly affecting macrophage M2-like polarization, supporting it as a promising therapeutic target against DLBCL.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"83 ","pages":"Article 102042"},"PeriodicalIF":2.3,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144638500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell sequencing revealed the recurrence causes of ETV6:RUNX1 fusion-positive B-ALL in children","authors":"Guotao Guan ,&nbsp;Xiuxiu Wang ,&nbsp;Xiuxin Li ,&nbsp;Qi Wang ,&nbsp;Xiuli Li ,&nbsp;Xiaojun Sun ,&nbsp;Liying Liu ,&nbsp;Yunfeng Lu ,&nbsp;Bingju Liu ,&nbsp;Xinyu Li ,&nbsp;Ping Zhao ,&nbsp;Fei Gao ,&nbsp;Lijun Chen ,&nbsp;Lihua Zhao ,&nbsp;Yunpeng Dai","doi":"10.1016/j.mcp.2025.102041","DOIUrl":"10.1016/j.mcp.2025.102041","url":null,"abstract":"<div><h3>Objective</h3><div>The ETV6RUNX1 fusion is the most common genetic abnormality in childhood B-cell acute lymphoblastic leukemia (B-ALL), yet nearly 50 % of relapses occur in patients initially classified as low-risk with this alteration. This study aimed to unravel the underlying pathways driving relapse in ETV6RUNX1 positive B-ALL.</div></div><div><h3>Methods</h3><div>Single-cell RNA sequencing (scRNA-seq) was performed on a cohort of four B-ALL patients with the ETV6RUNX1 fusion (three newly diagnosed and one relapsed case, selected from 25 patients).</div></div><div><h3>Results</h3><div>we discovered that relapsed samples exhibited a decline in T cell populations, an increase in CD8 Tex cells and B cells, and a higher proportion of malignant cells. Gene enrichment analysis demonstrated that IFN-γ response signaling pathways and inflammatory responses were significantly enriched in newly diagnosed samples. Conversely, the relapsed samples showed enrichment in the oxidative phosphorylation and glycolysis pathways. Additionally, analysis of cellular interactions revealed that malignant B cells could interact with T cells through LGALS9-HAVCR2, potentially leading to the exhaustion of effector T cells. Moreover, NPDC1, LEF1, and ERG exhibited higher activity levels in malignant B cells from relapsed patients, highlighting their roles in the progression and maintenance of leukemia.</div></div><div><h3>Conclusion</h3><div>In summary, our study provides valuable insights into the potential causes of relapse in B-ALL patients with ETV6RUNX1, providing a foundation for the identification of prospective therapeutic targets.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"83 ","pages":"Article 102041"},"PeriodicalIF":2.3,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144631140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of CPLX1 expression as a potential prognostic marker in colorectal cancer","authors":"Li Jin ,&nbsp;Lili Qian ,&nbsp;Xin Zhang ,&nbsp;Ting Liu","doi":"10.1016/j.mcp.2025.102040","DOIUrl":"10.1016/j.mcp.2025.102040","url":null,"abstract":"<div><h3>Objectives</h3><div>CPLX1 is a member of the complexin/Synaphin family. Studies have shown that CPLX1 is involved in tumor progression. However, the biological mechanism by which CPLX1 is involved in colorectal cancer (CRC) is unclear.</div></div><div><h3>Methods</h3><div>TIMER and TCGA database provided difference expression of CPLX1 mRNA in pan-cancer and CRC. We collected 90 cases of CRC and adjacent normal tissues for immunohistochemistry (IHC) and investigated CPLX1 protein expression and its correlation with clinical information. Cox regression and Kaplan–Meier were conducted to determine prognostic value of CPLX1 expression. We utilized Spearman analysis to explore the association between CPLX1 and immune cell infiltration, immune checkpoints. We utilized GSEA to investigate the biological molecular function for CPLX1 in CRC.</div></div><div><h3>Results</h3><div>CPLX1 mRNA expression was elevated in several cancers, including CRC. Elevated CPLX1 protein expression was confirmed by IHC in CRC samples, and showed a positive association with T stage. The survival analysis demonstrated that CPLX1 overexpression was linked to a poorer overall survival (OS), disease-specific survival (DSS), and progress-free interval (PFI) for CRC. Time ROC analysis suggested that the survival rate of 1-year, 2-year and 3-year for OS, DSS, and PFI was above 0.5, suggesting a certain prognostic value in CRC. Cox regression considered CPLX1 expression as a good prognostic index for predicting OS, DSS, and PFI. Furthermore, CPLX1 expression was associated with immunity in CRC. Functional analysis showed that CPLX1 related genes had participation in Notch signaling pathway.</div></div><div><h3>Conclusions</h3><div>CPLX1 was a latent prognostic and diagnostic marker for CRC and may also be a potential therapeutic target.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"83 ","pages":"Article 102040"},"PeriodicalIF":2.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress in the pathogenesis and treatment of pituitary neuroendocrine tumors (PitNETs): From molecular mechanisms to emerging therapies","authors":"Na Wu ,&nbsp;Naijia Wu ,&nbsp;Nan Wang ,&nbsp;Yonghong Zhu","doi":"10.1016/j.mcp.2025.102039","DOIUrl":"10.1016/j.mcp.2025.102039","url":null,"abstract":"<div><div>Pituitary neuroendocrine tumors (PitNETs), arising from anterior pituitary neuroendocrine cells, constitute 10–15 % of intracranial tumors. Though mostly benign, their location near critical structures like the optic chiasm and cavernous sinus causes severe neuroendocrine dysfunctions and mass effects. The 2022 WHO classification rebranded them from \"pituitary adenomas\" to emphasize their neuroendocrine lineage, yet challenges in prognostic prediction retain traditional terminology. Pathogenesis involves genetic mutations GNAS in GH-PitNETs, USP8 in ACTH-PitNETs), epigenetic dysregulation (METTL3-mediated m6A methylation), and signaling pathway aberrations (cAMP-PKA activation). Current treatments—surgery, dopamine agonists, somatostatin analogs, and radiation—face limitations like recurrence and side effects. Emerging strategies include targeted therapies (BET inhibitors) and immune checkpoint blockade, but tumor heterogeneity and lack of predictive biomarkers remain key obstacles. This review synthesizes pathogenesis, therapeutic advances, and research gaps to foster precision medicine and novel diagnostic/treatment paradigms for PitNETs.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"83 ","pages":"Article 102039"},"PeriodicalIF":2.3,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144530737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of cancer-associated fibroblast signature genes in ovarian cancer patients: impact on immunity, drug resistance, and prognosis","authors":"Shunjin Zhang ,&nbsp;Jiazhuo Yan ,&nbsp;Wenjing Pan ,&nbsp;Chaoyang Jia ,&nbsp;Wei Liu ,&nbsp;Sijia Liu ,&nbsp;Zhao Wang ,&nbsp;Yujie Liu ,&nbsp;Yunyan Zhang","doi":"10.1016/j.mcp.2025.102038","DOIUrl":"10.1016/j.mcp.2025.102038","url":null,"abstract":"<div><div>Ovarian cancer (OC) is women's third most common gynecologic tumor and is highly lethal. Cancer-associated fibroblasts (CAFs) are associated with cancer at all stages of disease progression and are involved in biological processes, including inflammatory processes, tumor development occurrence, and immune rejection. This study aimed to construct prognosis-related CAFs regulatory factors to predict the survival of OC patients. Datasets of OC patients with complete clinical information were collected from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) databases. First, we identified potential regulator factors of CAFs in OC based on the xCell algorithm and weighted gene co-expression analysis (WGCNA). Further screening using one-way cox regression analysis and LASSO regression models yielded 22 prognosis-related CAFs regulatory factors, using which a model was constructed. Subsequently, the diagnostic effectiveness of the model was assessed using receiver operating characteristic (ROC) curves, and the validity of the CAFs regulatory factors survival model was verified in three additional independent datasets and single cell data. Meanwhile, experimental validation was conducted using immunohistochemistry and Western blot. The results showed that GAS1 (Growth arrest specific 1) exhibited a higher expression pattern in fibroblasts from ovarian cancer patients.</div><div>The assessment of resistance and immune checkpoint differences across various risk score groups indicates that the CAFs regulatory factor survival model is practical for guiding systemic treatment. In summary, this study establishes a prognostic model composed of 22 CAFs regulatory factors to predict the prognosis of ovarian cancer (OC), providing new perspectives for the clinical treatment of OC.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"83 ","pages":"Article 102038"},"PeriodicalIF":2.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-130 as a critical modulator of cardiac remodeling: interplay between autophagic flux and ferroptotic pathways in acute myocardial infarction","authors":"Liang Chen ,&nbsp;Dongyang Jiang ,&nbsp;Wenxin Kou ,&nbsp;Yawei Xu","doi":"10.1016/j.mcp.2025.102037","DOIUrl":"10.1016/j.mcp.2025.102037","url":null,"abstract":"<div><h3>Background</h3><div>Acute myocardial infarction (AMI) continues to be a leading cause of morbidity and death.</div></div><div><h3>Objective</h3><div>This study investigates <em>miR-130</em>'s regulatory mechanisms in AMI progression.</div></div><div><h3>Methods</h3><div>Bioinformatics analysis of <em>miR-130</em> conservation and differential expression was performed using miRbase and Gene Expression Omnibus datasets. Angiotensin II (Ang II)-treated H9C2 cardiomyocytes modeled AMI in vitro. <em>miR-130</em> inhibitor/mimic transfection, combined with autophagy inhibitor Spautin-1 or ferroptosis inhibitor Ferrostatin-1, were assessed via qPCR, ELISA (PC III, HA, CTnT, CK-MB), Western blot (LC3-II/LC3-I, p62, SLC7A11, GPX4), and flow cytometry.</div></div><div><h3>Results</h3><div>Our results demonstrate that Ang II stimulation significantly elevates <em>miR-130</em> expression in H9C2 cells, concomitant with increased secretion of myocardial injury and fibrosis markers. Inhibition of <em>miR-130</em> markedly improved cell viability and reduced apoptosis, accompanied by decreased expression of fibrosis markers such as α-SMA and Collagen I, and a rebalancing of autophagy dynamics, as indicated by an increased LC3-II/LC3-I ratio and elevated p62 levels. Conversely, <em>miR-130</em> overexpression via a synthetic mimic reduced cell viability and enhanced apoptosis, with a corresponding rise in fibrosis markers (PC III, HA, CTnT, CK-MB) and disruption of both autophagy and ferroptosis pathways, evidenced by decreased levels of SLC7A11 and GPX4. Notably, the adverse effects induced by <em>miR-130</em> mimic were effectively reversed by Spautin-1 and Ferrostatin-1 co-treatment, suggesting that <em>miR-130</em> modulates AMI-related cellular responses through intertwined autophagy and ferroptosis mechanisms.</div></div><div><h3>Conclusion</h3><div>These findings reveal that <em>miR-130</em> is a pivotal regulator of myocardial injury in AMI, mediating its effects via the modulation of autophagy and ferroptosis pathways. Targeting <em>miR-130</em> may therefore represent a promising therapeutic strategy for mitigating myocardial damage and improving cardiac function following AMI.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"83 ","pages":"Article 102037"},"PeriodicalIF":2.3,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNMT3A triggers tumorigenesis of non-small cell lung cancer through regulation of SLIT2 methylation and SLIT2-mediated macrophage M1/M2 polarization","authors":"Tian-xing Ni ,&nbsp;Jia-bo Shen","doi":"10.1016/j.mcp.2025.102033","DOIUrl":"10.1016/j.mcp.2025.102033","url":null,"abstract":"<div><h3>Background</h3><div>Increased DNA methylation is prevalent in human cancers and is one of the important characteristics of tumors. This research aims to investigate the molecular mechanisms that involve DNMT3A and DNA methylation modification of SLIT2 in non-small cell lung cancer (NSCLC).</div></div><div><h3>Methods</h3><div>Gene expression was examined using Western blot assay, immunohistochemistry and RT-qPCR. Cell viability and motility were measured by CCK-8, colony formation, Transwell and wound healing assays. Macrophage M1/M2 polarization was assessed through a flow cytometry assay. Using ELISA, the secretion levels of inflammatory factors by macrophage M1/M2 polarization were determined. ChIP, qMSP and dual-luciferase reporter assays confirmed the relationship between DNMT3A and SLIT2.</div></div><div><h3>Results</h3><div>High expression of DNMT3A was observed in NSCLC patients, enhancing NSCLC cell viability and metastasis. Mechanically, DNMT3A was identified to target SLIT2. DNMT3A inhibited SLIT2 expression through DNA methylation modification in NSCLC. Further, overexpression of SLIT2 impeded M2 polarization of macrophages in NSCLC. And SLIT2 overexpression hindered NSCLC tumor growth <em>in vivo</em> by affecting macrophage M2 polarization. Finally, DNMT3A was found to promote the progression of NSCLC by downregulating SLIT2.</div></div><div><h3>Conclusion</h3><div>DNMT3A promotes the progression of NSCLC via regulating methylation modification of SLIT2 and SLIT2-mediated macrophage M1/M2 polarization.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"82 ","pages":"Article 102033"},"PeriodicalIF":2.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144188363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gastrodin promotes osteogenic differentiation by stimulating the Wnt/β-catenin signaling pathway","authors":"Wei Jiang ,&nbsp;Lifeng Zhang ,&nbsp;Wenshan Shan ,&nbsp;Zuomeng Wu ,&nbsp;Jiaqi Wang ,&nbsp;Cailiang Shen","doi":"10.1016/j.mcp.2025.102035","DOIUrl":"10.1016/j.mcp.2025.102035","url":null,"abstract":"<div><h3>Background</h3><div>Osteoporosis is a common disease that can lead to fracture as well as various skeletal symptoms and is a global health problem. Traditional Chinese medicine (TCM) may offer novel approaches for treating osteoporosis. Our study aimed to investigate the osteogenic potential and underlying mechanisms of gastrodin in promoting osteogenic differentiation.</div></div><div><h3>Methods</h3><div>By combining network pharmacology and bioinformatics, we conducted experiments to inspect cell viability, Alkaline Phosphatase (ALP) viability, and Alizarin red staining (ARS) and investigate the expression profiles of genes and proteins relevant to osteogenesis, including β-catenin, Runt-related transcription factor 2 (Runx2), Low Density Lipoprotein Receptor-Related Protein 5 (LRP5) and Glycogen synthase kinase-3 beta (GSK-3β). Statistical analysis was used for validation.</div></div><div><h3>Results</h3><div>Network pharmacology and bioinformatics analyses revealed that gastrodin might influence osteogenic differentiation. The experimental results revealed that gastrodin had no toxic effects and was able to promote ALP activity and stimulate osteogenic differentiation of Mouse Calvaria-derived Osteoblastic Cell Line.</div><div>(MC3T3-E1) cells. Subsequent network pharmacology and bioinformatics studies revealed that gastrodin might affect osteogenic differentiation through the Wnt/β-catenin signaling pathway. The results revealed that gastrodin influenced osteogenic differentiation genes and protein expression, including the upregulation of β-catenin, Runx2, and LRP5 and the downregulation of GSK-3β, and Dickkopf-1 (DKK-1) inhibited its promotion.</div></div><div><h3>Conclusion</h3><div>Gastrodin enhances the Wingless (Wnt)/β-catenin signaling pathway by increasing β-catenin accumulation and nuclear migration as well as decreasing GSK-3β, which increases Runx2 expression, consequently encouraging MC3T3-E1 cell osteogenic differentiation, and may be applied as a potential drug for osteoporosis therapy and prevention.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"82 ","pages":"Article 102035"},"PeriodicalIF":2.3,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144175376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}