Pub Date : 2026-02-06DOI: 10.1016/j.mcp.2026.102064
Xue Wang, Wenjun Wang, Ran Yao, Zhao Liu, Qianqing Wang
Stem cell-derived and plant-derived exosomes are emerging as promising therapeutic agents in cutaneous repair, regeneration, and rejuvenation. They facilitate wound healing and skin revitalization through multifaceted mechanisms, including immunomodulation, promotion of cellular differentiation, and stimulation of angiogenesis. Additionally, their ability to modulate collagen production and remodeling underscores their potential in addressing skin aging and improving cosmetic outcomes. Consequently, exosome-based therapies show promise for a range of conditions, from challenging wounds and skin aging to pigmentary disorders, hair loss, certain immune-mediated dermatoses. To ensure a comprehensive and unbiased synthesis of the current evidence, this systematic review was conducted following a structured methodology, encompassing a search across multiple major databases over a defined 20-year period. This review systematically outlines the roles and applications of commonly employed plant exosomes and stem cell exosomes in recent years' advancements in skin repair and cosmetic dermatology. By synthesizing the current understanding of their mechanisms and clinical potential, this review aims to highlight viable therapeutic strategies that bridge the gap between medical dermatology and aesthetic medicine.
{"title":"Stem Cell-Derived and Plant-Derived Exosomes: Promising Therapeutics for Skin Healing and Regeneration.","authors":"Xue Wang, Wenjun Wang, Ran Yao, Zhao Liu, Qianqing Wang","doi":"10.1016/j.mcp.2026.102064","DOIUrl":"https://doi.org/10.1016/j.mcp.2026.102064","url":null,"abstract":"<p><p>Stem cell-derived and plant-derived exosomes are emerging as promising therapeutic agents in cutaneous repair, regeneration, and rejuvenation. They facilitate wound healing and skin revitalization through multifaceted mechanisms, including immunomodulation, promotion of cellular differentiation, and stimulation of angiogenesis. Additionally, their ability to modulate collagen production and remodeling underscores their potential in addressing skin aging and improving cosmetic outcomes. Consequently, exosome-based therapies show promise for a range of conditions, from challenging wounds and skin aging to pigmentary disorders, hair loss, certain immune-mediated dermatoses. To ensure a comprehensive and unbiased synthesis of the current evidence, this systematic review was conducted following a structured methodology, encompassing a search across multiple major databases over a defined 20-year period. This review systematically outlines the roles and applications of commonly employed plant exosomes and stem cell exosomes in recent years' advancements in skin repair and cosmetic dermatology. By synthesizing the current understanding of their mechanisms and clinical potential, this review aims to highlight viable therapeutic strategies that bridge the gap between medical dermatology and aesthetic medicine.</p>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":" ","pages":"102064"},"PeriodicalIF":3.0,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146143777","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}
Cancer arises and is resistant to therapy via intricate molecular networks that are poorly characterised. While individually, Cullin-3 (CUL3) and circular RNAs (circRNAs) have been reported to modulate cancer, their synergistic effect in the modulation of tyrosine kinase inhibitor (TKI) resistance is yet to be studied. An emerging circRNA-CUL3-TKI regulatory framework is highlighted as a potential contributor to oncogenesis and drug sensitivity in this review. We discuss how circRNA-associated networks may influence CUL3-dependent pathways implicated in tumour resistance to therapy by modulating autophagy, ferroptosis, stress-responses, and redox signalling. Exosomal circRNAs and circRNAs of the CUL3 gene itself are highlighted as dynamic mediators of resistance as well as biomarkers. How they interact with Kelch-like ECH-associated protein 1- Nuclear factor erythroid 2-related factor 2 (KEAP1-NRF2) signalling reveals that they enhance tumour survival under therapy pressure. By highlighting key processes of carcinogenesis and resistance, the circRNA-CUL3-TKI axis represents a testable therapeutic framework. Modeling circRNA networks, predicting TKI response, finding biomarkers, and developing personalised treatment plans are all made possible by applications of artificial intelligence and machine learning (AI/ML), as explored in this review. Antisense oligonucleotides, Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-based molecules, neddylation inhibitors or PROteolysis TArgeting Chimera (PROTACs) are examples of potential interventions that, when combined with AI/ML techniques, improve therapeutic efficacy and may inform future desensitisation strategies. These collectively emphasize the emerging applications for AI/ML in understanding the circRNA-CUL3-TKI crosstalk and developing methods to resensitize cancers that are resistant to therapy.
{"title":"Emerging roles of artificial intelligence/machine learning (AI/ML) towards new understandings in molecular crosstalk between circRNA-CUL3-TKI to resensitize chemoresistant cancers.","authors":"Pranjali Dutta, Samiksha Middya, Siddharth Shome, Manshi Kumari Gupta, Poobana Dharmalingam, C Sudandiradoss","doi":"10.1016/j.mcp.2026.102063","DOIUrl":"10.1016/j.mcp.2026.102063","url":null,"abstract":"<p><p>Cancer arises and is resistant to therapy via intricate molecular networks that are poorly characterised. While individually, Cullin-3 (CUL3) and circular RNAs (circRNAs) have been reported to modulate cancer, their synergistic effect in the modulation of tyrosine kinase inhibitor (TKI) resistance is yet to be studied. An emerging circRNA-CUL3-TKI regulatory framework is highlighted as a potential contributor to oncogenesis and drug sensitivity in this review. We discuss how circRNA-associated networks may influence CUL3-dependent pathways implicated in tumour resistance to therapy by modulating autophagy, ferroptosis, stress-responses, and redox signalling. Exosomal circRNAs and circRNAs of the CUL3 gene itself are highlighted as dynamic mediators of resistance as well as biomarkers. How they interact with Kelch-like ECH-associated protein 1- Nuclear factor erythroid 2-related factor 2 (KEAP1-NRF2) signalling reveals that they enhance tumour survival under therapy pressure. By highlighting key processes of carcinogenesis and resistance, the circRNA-CUL3-TKI axis represents a testable therapeutic framework. Modeling circRNA networks, predicting TKI response, finding biomarkers, and developing personalised treatment plans are all made possible by applications of artificial intelligence and machine learning (AI/ML), as explored in this review. Antisense oligonucleotides, Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-based molecules, neddylation inhibitors or PROteolysis TArgeting Chimera (PROTACs) are examples of potential interventions that, when combined with AI/ML techniques, improve therapeutic efficacy and may inform future desensitisation strategies. These collectively emphasize the emerging applications for AI/ML in understanding the circRNA-CUL3-TKI crosstalk and developing methods to resensitize cancers that are resistant to therapy.</p>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":" ","pages":"102063"},"PeriodicalIF":3.0,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101023","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}
Pub Date : 2026-01-23DOI: 10.1016/j.mcp.2026.102061
Longfei Fan , Zhaoying Wang , Tao Tao , Dongdong Huang , Xiaoyun Tang , Rui Wang , Zhongqiang Qin , Bo Xie , Yi Tan
Purpose
This investigation seeks to examine the relationship between exosomal Insulin-like Growth Factor Binding Protein Acid Labile Subunit (IGFALS) gene expression, immune infiltration, and clinical outcomes in individuals with hepatocellular carcinoma (HCC).
Method
Clinical data and IGFALS expression levels were obtained from the TCGA and GEO databases. Immunohistochemistry was performed to confirm IGFALS expression in both HCC and adjacent non-tumor tissues. To validate survival analyses, restricted cubic spline models were used to explore associations between overall survival (OS) and the expression of IGFALS in liver hepatocellular carcinoma (LIHC). Gene set enrichment analysis (GSEA) identified IGFALS-associated pathways, while Gene set enrichment analysis (ssGSEA) evaluated IGFALS-immune cell infiltration correlations. Functional characterization included proliferation, migration/invasion, molecular profiling, and apoptosis assays.
Result
Compared to normal tissues, IGFALS expression levels were notably decreased in tumor tissues. A notable link was detected between IGFALS expression and multiple clinical factors, including gender, weight, residual tumor, adjacent hepatic tissue inflammation, vascular invasion, AFP, BCLC, tumor size, multinodular, TACE, and satellite lesion in HCC. Reduced IGFALS expression in HCC was correlated with decreased OS. Moreover, the IGFALS level in malignant tumor cells post-immunotherapy was observed to be markedly higher than that in the pre-treatment phase. A strong association between IGFALS and immune infiltration levels was also established. At the same time, in vitro experiments also verified the function of the IGFALS gene.
Conclusion
The exosomal IGFALS gene holds potential as a prospective indicator for assessing the outcome of individuals with HCC.
{"title":"Exosomal IGFALS as a prognostic biomarker in hepatocellular Carcinoma: Associations with immune infiltration and clinical outcomes","authors":"Longfei Fan , Zhaoying Wang , Tao Tao , Dongdong Huang , Xiaoyun Tang , Rui Wang , Zhongqiang Qin , Bo Xie , Yi Tan","doi":"10.1016/j.mcp.2026.102061","DOIUrl":"10.1016/j.mcp.2026.102061","url":null,"abstract":"<div><h3>Purpose</h3><div>This investigation seeks to examine the relationship between exosomal Insulin-like Growth Factor Binding Protein Acid Labile Subunit (IGFALS) gene expression, immune infiltration, and clinical outcomes in individuals with hepatocellular carcinoma (HCC).</div></div><div><h3>Method</h3><div>Clinical data and IGFALS expression levels were obtained from the TCGA and GEO databases. Immunohistochemistry was performed to confirm IGFALS expression in both HCC and adjacent non-tumor tissues. To validate survival analyses, restricted cubic spline models were used to explore associations between overall survival (OS) and the expression of IGFALS in liver hepatocellular carcinoma (LIHC). Gene set enrichment analysis (GSEA) identified IGFALS-associated pathways, while Gene set enrichment analysis (ssGSEA) evaluated IGFALS-immune cell infiltration correlations. Functional characterization included proliferation, migration/invasion, molecular profiling, and apoptosis assays.</div></div><div><h3>Result</h3><div>Compared to normal tissues, IGFALS expression levels were notably decreased in tumor tissues. A notable link was detected between IGFALS expression and multiple clinical factors, including gender, weight, residual tumor, adjacent hepatic tissue inflammation, vascular invasion, AFP, BCLC, tumor size, multinodular, TACE, and satellite lesion in HCC. Reduced IGFALS expression in HCC was correlated with decreased OS. Moreover, the IGFALS level in malignant tumor cells post-immunotherapy was observed to be markedly higher than that in the pre-treatment phase. A strong association between IGFALS and immune infiltration levels was also established. At the same time, in vitro experiments also verified the function of the IGFALS gene.</div></div><div><h3>Conclusion</h3><div>The exosomal IGFALS gene holds potential as a prospective indicator for assessing the outcome of individuals with HCC.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"86 ","pages":"Article 102061"},"PeriodicalIF":3.0,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047280","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}
Pub Date : 2025-12-26DOI: 10.1016/j.mcp.2025.102060
Yangchun Zhang , Xu Li , Yifei Liu , Yongxu Wu , Chunlei Li , Chunlin Zhang , Zhaohui Liu
Background
Head and neck squamous cell carcinoma (HNSCC) remains a prevalent malignancy worldwide, posing significant health threats due to its high recurrence and metastatic potential. HPV-positive and negative HNSCC subtypes exhibit distinct prognostic profiles and their underlying pathogenic mechanisms remain poorly characterized.
Methods
Four HNSCC cell lines were selected: two HPV-positive (UM-SCC-47 and UPCI-SCC-090) and two HPV-negative (FaDu and UM-SCC-4). Basal miR-106a expression was measured in HPV-positive and -negative cells, followed by RT-qPCR validation of miR-106a, HPV-E7, RUNX3 overexpression and knockdown efficiency. Functional assays included CCK-8 for proliferation, wound healing for migration, Transwell for invasion, and flow cytometry for apoptosis. RT-qPCR quantified HPV-E7, miR-106a, RUNX3, and TGF-β1 mRNA levels; RUNX3 and TGF-β1 protein expression was assessed via Western blot. Dual-luciferase reporter assays confirmed the direct targeting of miR-106a to RUNX3. Finally, xenograft nude mouse models assessed miR-106a's effects on tumor growth and downstream molecular regulation in HPV-positive and -negative HNSCC.
Results
Comparative analysis revealed that miR-106a was significantly upregulated in HPV-positive HNSCC cells compared to their HPV-negative counterparts. Functional assays demonstrated that miR-106a overexpression enhanced HNSCC cell proliferation, migration, and invasion while suppressing apoptosis, whereas ectopic expression of RUNX3 exerted opposing effects on these oncogenic phenotypes. Mechanistically, miR-106a overexpression transcriptionally downregulated RUNX3 and concurrently elevated TGF-β1 expression, while RUNX3 overexpression inversely suppressed TGF-β1 levels. Dual-luciferase reporter assays confirmed a direct binding interaction between miR-106a and the 3′UTR of RUNX3. Rescue experiments further established that HPV E7-driven oncogenic effects—enhanced proliferation, migration, invasion, and apoptosis suppression—were abrogated by miR-106a inhibition, concomitant with restored expression of RUNX3 and attenuated TGF-β1 signaling. In vivo studies corroborated these findings, showing that miR-106a overexpression accelerated tumor growth in xenograft models, accompanied by progressive RUNX3 downregulation and TGF-β1 upregulation, consistent with its in vitro regulatory axis.
Conclusions
Our findings suggest that the E7/miR-106a/RUNX3/TGF-β1 axis modulates proliferation, migration, invasion, and apoptosis in HPV-positive versus negative HNSCC, implicating its pathogenic role in tumor progression.
{"title":"The HPV-E7/miR-106a/RUNX3/TGF-β1 axis regulates malignant progression in both HPV-positive and negative head and neck squamous cell carcinoma","authors":"Yangchun Zhang , Xu Li , Yifei Liu , Yongxu Wu , Chunlei Li , Chunlin Zhang , Zhaohui Liu","doi":"10.1016/j.mcp.2025.102060","DOIUrl":"10.1016/j.mcp.2025.102060","url":null,"abstract":"<div><h3>Background</h3><div>Head and neck squamous cell carcinoma (HNSCC) remains a prevalent malignancy worldwide, posing significant health threats due to its high recurrence and metastatic potential. HPV-positive and negative HNSCC subtypes exhibit distinct prognostic profiles and their underlying pathogenic mechanisms remain poorly characterized.</div></div><div><h3>Methods</h3><div>Four HNSCC cell lines were selected: two HPV-positive (UM-SCC-47 and UPCI-SCC-090) and two HPV-negative (FaDu and UM-SCC-4). Basal miR-106a expression was measured in HPV-positive and -negative cells, followed by RT-qPCR validation of miR-106a, HPV-E7, RUNX3 overexpression and knockdown efficiency. Functional assays included CCK-8 for proliferation, wound healing for migration, Transwell for invasion, and flow cytometry for apoptosis. RT-qPCR quantified HPV-E7, miR-106a, RUNX3, and TGF-β1 mRNA levels; RUNX3 and TGF-β1 protein expression was assessed via Western blot. Dual-luciferase reporter assays confirmed the direct targeting of miR-106a to RUNX3. Finally, xenograft nude mouse models assessed miR-106a's effects on tumor growth and downstream molecular regulation in HPV-positive and -negative HNSCC.</div></div><div><h3>Results</h3><div>Comparative analysis revealed that miR-106a was significantly upregulated in HPV-positive HNSCC cells compared to their HPV-negative counterparts. Functional assays demonstrated that miR-106a overexpression enhanced HNSCC cell proliferation, migration, and invasion while suppressing apoptosis, whereas ectopic expression of RUNX3 exerted opposing effects on these oncogenic phenotypes. Mechanistically, miR-106a overexpression transcriptionally downregulated RUNX3 and concurrently elevated TGF-β1 expression, while RUNX3 overexpression inversely suppressed TGF-β1 levels. Dual-luciferase reporter assays confirmed a direct binding interaction between miR-106a and the 3′UTR of RUNX3. Rescue experiments further established that HPV E7-driven oncogenic effects—enhanced proliferation, migration, invasion, and apoptosis suppression—were abrogated by miR-106a inhibition, concomitant with restored expression of RUNX3 and attenuated TGF-β1 signaling. In vivo studies corroborated these findings, showing that miR-106a overexpression accelerated tumor growth in xenograft models, accompanied by progressive RUNX3 downregulation and TGF-β1 upregulation, consistent with its in vitro regulatory axis.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that the E7/miR-106a/RUNX3/TGF-β1 axis modulates proliferation, migration, invasion, and apoptosis in HPV-positive versus negative HNSCC, implicating its pathogenic role in tumor progression.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"85 ","pages":"Article 102060"},"PeriodicalIF":3.0,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145851392","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}
Acute myeloid leukemia (AML) is a highly diverse malignant tumor at the molecular level with a high mortality rate. However, its underlying mechanisms remain poorly understood, and reliable biomarkers are lacking.
Methods
AML-related biomarkers were identified through a comprehensive analysis of single-cell RNA sequencing (scRNA-seq), Mendelian randomization (MR), and gene regulatory networks. The biomarkers were then subjected to GSEA enrichment analysis and in vitro experimental validation.
Results
scRNA-seq identified a total of 22,742 cells with detectable gene expression. Among the differentially expressed genes in the cells, 174 marker genes were screened out. MR analysis of marker genes showed that ITGB2, AIF1, CA2, CST7, and JCHAIN had a significant causal relationship with AML. Cumulative recovery curve analysis showed that AIF1, CST7, and ITGB2 were in the top motifs with the highest normalized enrichment scores. Therefore, they were recorded as biomarkers. Cellular experiments confirmed that AIF1, CST7, and ITGB2 promote cell proliferation and inhibit apoptosis.
Conclusion
This study identified AIF1, CST7, and ITGB2 as biomarkers for AML through scRNA-seq, MR, and transcription factor enrichment analysis. Additionally, in vitro experiments, including cell transfection, cell proliferation, and flow cytometry, validated the important role of these biomarkers in promoting the malignant phenotype of AML.
{"title":"Identification and experimental validation of biomarkers for acute myeloid leukemia based on single-cell RNA sequencing data","authors":"Xin Yang, Siyue Zhou, Yuanju Chen, Ying Wang, Yujing Cheng, Chan Zhang, Qi Li","doi":"10.1016/j.mcp.2025.102059","DOIUrl":"10.1016/j.mcp.2025.102059","url":null,"abstract":"<div><h3>Background</h3><div>Acute myeloid leukemia (AML) is a highly diverse malignant tumor at the molecular level with a high mortality rate. However, its underlying mechanisms remain poorly understood, and reliable biomarkers are lacking.</div></div><div><h3>Methods</h3><div>AML-related biomarkers were identified through a comprehensive analysis of single-cell RNA sequencing (scRNA-seq), Mendelian randomization (MR), and gene regulatory networks. The biomarkers were then subjected to GSEA enrichment analysis and in vitro experimental validation.</div></div><div><h3>Results</h3><div>scRNA-seq identified a total of 22,742 cells with detectable gene expression. Among the differentially expressed genes in the cells, 174 marker genes were screened out. MR analysis of marker genes showed that ITGB2, AIF1, CA2, CST7, and JCHAIN had a significant causal relationship with AML. Cumulative recovery curve analysis showed that AIF1, CST7, and ITGB2 were in the top motifs with the highest normalized enrichment scores. Therefore, they were recorded as biomarkers. Cellular experiments confirmed that AIF1, CST7, and ITGB2 promote cell proliferation and inhibit apoptosis.</div></div><div><h3>Conclusion</h3><div>This study identified AIF1, CST7, and ITGB2 as biomarkers for AML through scRNA-seq, MR, and transcription factor enrichment analysis. Additionally, in vitro experiments, including cell transfection, cell proliferation, and flow cytometry, validated the important role of these biomarkers in promoting the malignant phenotype of AML.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"85 ","pages":"Article 102059"},"PeriodicalIF":3.0,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145835245","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}
Pub Date : 2025-12-01DOI: 10.1016/j.mcp.2025.102057
Xin Chen, Weiqing Chen
Background
Diffuse large B cell lymphoma (DLBCL) is a heterogeneous malignancy with an unidentified molecular etiology. This study aims to investigate the role of DEAD-box helicase 10 (DDX10), a novel carcinogenic gene, in DLBCL.
Methods
The expression of DDX10 in DLBCL was analyzed by the GEPIA2 bioinformatics tool. DDX10 and fibrillarin (FBL) expressions in DLBCL patients’ cancer tissues and cell lines were measured via quantitative real-time reverse transcription polymerase chain reaction. RNA immunoprecipitation assay was used to confirm FBL-DDX10 interaction. The effects of DDX10/FBL overexpression and knockdown on cell viability, invasion, and Wnt/β-catenin pathway proteins were evaluated in DLBCL cell lines.
Results
DDX10 and FBL exhibited elevated expression levels in patients with DLBCL, particularly in those with stage III or IV DLBCL. DDX10 can bind to FBL in DLBCL cells. Silencing of DDX10 or FBL suppressed viability, proliferation and invasion, and downregulated the expressions of β-catenin, cyclin D1, and c-Myc proteins in DLBCL cells. The regulatory impact of DDX10 or FBL silencing on DLBCL cells was counteracted by the overexpression of FBL or DDX10.
Conclusion
DDX10 contributes to the proliferation and invasion of DLBCL cells via positively regulating FBL, highlighting the DDX10–FBL axis as a potential therapeutic target. This work provides new insights into DLBCL pathogenesis and underscores the biomedical relevance of targeting DDX10–FBL.
{"title":"Reveal the regulatory role of DDX10 in diffuse large B-cell lymphoma: binding with FBL to promote cell proliferation and invasion","authors":"Xin Chen, Weiqing Chen","doi":"10.1016/j.mcp.2025.102057","DOIUrl":"10.1016/j.mcp.2025.102057","url":null,"abstract":"<div><h3>Background</h3><div>Diffuse large B cell lymphoma (DLBCL) is a heterogeneous malignancy with an unidentified molecular etiology. This study aims to investigate the role of DEAD-box helicase 10 (DDX10), a novel carcinogenic gene, in DLBCL.</div></div><div><h3>Methods</h3><div>The expression of DDX10 in DLBCL was analyzed by the GEPIA2 bioinformatics tool. DDX10 and fibrillarin (FBL) expressions in DLBCL patients’ cancer tissues and cell lines were measured via quantitative real-time reverse transcription polymerase chain reaction. RNA immunoprecipitation assay was used to confirm FBL-DDX10 interaction. The effects of DDX10/FBL overexpression and knockdown on cell viability, invasion, and Wnt/β-catenin pathway proteins were evaluated in DLBCL cell lines.</div></div><div><h3>Results</h3><div>DDX10 and FBL exhibited elevated expression levels in patients with DLBCL, particularly in those with stage III or IV DLBCL. DDX10 can bind to FBL in DLBCL cells. Silencing of DDX10 or FBL suppressed viability, proliferation and invasion, and downregulated the expressions of β-catenin, cyclin D1, and c-Myc proteins in DLBCL cells. The regulatory impact of DDX10 or FBL silencing on DLBCL cells was counteracted by the overexpression of FBL or DDX10.</div></div><div><h3>Conclusion</h3><div>DDX10 contributes to the proliferation and invasion of DLBCL cells via positively regulating FBL, highlighting the DDX10–FBL axis as a potential therapeutic target. This work provides new insights into DLBCL pathogenesis and underscores the biomedical relevance of targeting DDX10–FBL.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"85 ","pages":"Article 102057"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145665704","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}
Pub Date : 2025-11-17DOI: 10.1016/j.mcp.2025.102056
Qian Wei , Ze Li , Honglei Feng , Jingya Zhang , Lijuan Wei
Introduction
Pancreatic cancer (PC) remains one of the most lethal malignancies worldwide, creating a critical need for reliable prognostic biomarkers, particularly those reflecting tumor microenvironment dynamics.
Methods
We investigated the combined prognostic value of a composite inflammatory prognostic model for PC progression. A retrospective cohort analysis of 171 patients with PC was conducted using receiver operating characteristic (ROC) curve analysis, along with univariate and multivariate Cox regression analyses. Survival curves were plotted using the Kaplan-Meier method. A clinical prognostic nomogram was constructed based on independent prognostic factors.
Results
ROC curve analysis demonstrated that C-reactive protein-to-lymphocyte ratio (CLR) had the highest predictive accuracy for 3-year survival. Survival analysis revealed that TNM stage, CA19-9, CEA, neutrophil count, CRP level, the neutrophil-to-lymphocyte ratio (NLR), and CLR were significantly associated with overall survival. Multivariate Cox regression analysis confirmed that advanced lymphatic metastasis, advanced TNM stage, elevated CA19-9, elevated CEA, elevated neutrophil count, elevated NLR, and elevated CLR were independent prognostic factors. The prognostic nomogram incorporating these variables exhibited robust discriminative capacity and well-calibrated predictions of survival. Using the inflammatory prognostic model, patients in the high-risk group had a significantly shorter median overall survival than those in the low-risk group, with strong predictive accuracy for 1-year and 3-year survival. Validation in a subgroup of patients with pancreatic ductal adenocarcinoma further supported the clinical utility of the model, showing superior 3-year predictive performance and a pronounced survival disparity between the risk groups.
Conclusions
A combination of inflammatory and clinical markers can effectively predict the prognosis of pancreatic cancer. The constructed composite inflammatory prognostic model demonstrated high clinical practical value and provided a reliable tool for individualized prognostic risk assessment.
{"title":"Prognostic value of composite inflammatory prognostic model in pancreatic cancer","authors":"Qian Wei , Ze Li , Honglei Feng , Jingya Zhang , Lijuan Wei","doi":"10.1016/j.mcp.2025.102056","DOIUrl":"10.1016/j.mcp.2025.102056","url":null,"abstract":"<div><h3>Introduction</h3><div>Pancreatic cancer (PC) remains one of the most lethal malignancies worldwide, creating a critical need for reliable prognostic biomarkers, particularly those reflecting tumor microenvironment dynamics.</div></div><div><h3>Methods</h3><div>We investigated the combined prognostic value of a composite inflammatory prognostic model for PC progression. A retrospective cohort analysis of 171 patients with PC was conducted using receiver operating characteristic (ROC) curve analysis, along with univariate and multivariate Cox regression analyses. Survival curves were plotted using the Kaplan-Meier method. A clinical prognostic nomogram was constructed based on independent prognostic factors.</div></div><div><h3>Results</h3><div>ROC curve analysis demonstrated that C-reactive protein-to-lymphocyte ratio (CLR) had the highest predictive accuracy for 3-year survival. Survival analysis revealed that TNM stage, CA19-9, CEA, neutrophil count, CRP level, the neutrophil-to-lymphocyte ratio (NLR), and CLR were significantly associated with overall survival. Multivariate Cox regression analysis confirmed that advanced lymphatic metastasis, advanced TNM stage, elevated CA19-9, elevated CEA, elevated neutrophil count, elevated NLR, and elevated CLR were independent prognostic factors. The prognostic nomogram incorporating these variables exhibited robust discriminative capacity and well-calibrated predictions of survival. Using the inflammatory prognostic model, patients in the high-risk group had a significantly shorter median overall survival than those in the low-risk group, with strong predictive accuracy for 1-year and 3-year survival. Validation in a subgroup of patients with pancreatic ductal adenocarcinoma further supported the clinical utility of the model, showing superior 3-year predictive performance and a pronounced survival disparity between the risk groups.</div></div><div><h3>Conclusions</h3><div>A combination of inflammatory and clinical markers can effectively predict the prognosis of pancreatic cancer. The constructed composite inflammatory prognostic model demonstrated high clinical practical value and provided a reliable tool for individualized prognostic risk assessment.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"84 ","pages":"Article 102056"},"PeriodicalIF":3.0,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145557565","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}
Pub Date : 2025-11-04DOI: 10.1016/j.mcp.2025.102055
Adrian Rombach , Maximilian Geissler , Liu Xiao , Lina-Elisabeth Qasem , Lena Stange , Vincent Prinz , Daniel Jussen , Somaya Landolsi , Konstantinos D. Kokkaliaris , Hind Medyouf , Lisa Sevenich , Pia Zeiner , Yvonne Reiss , Pinar Cakmak , Moritz Armbrust , Katharina J. Weber , Karl Heinz Plate , Stefan Offermanns , Thomas Broggini , Marcus Czabanka
Human tissue samples are a crucial resource for cancer research, offering key insights into physiological and pathological processes while enabling comprehensive characterization of molecular signatures across cancer subtypes. Recent advances in genetic analysis techniques lead to a substantiall expansion of specific molecular pathways knowledge. The application of these technologies to fresh tissue samples from patients undergoing surgical resection for metastatic disease represents a promising approach to gain a deeper understanding of the biology of brain metastasis. Brain metastases remain particularly challenging due to their poor prognosis and the complex mechanisms underlying central nervous system invasion. This study sought to identify preoperative factors influencing the research utility of fresh brain metastasis tissue samples. A pipeline was established to transfer fresh, surplus tissue from surgical resections to research laboratories with histological quality assessment. Of the fifty-five fresh specimens collected, thirty-eight (69 %) were classified as suitable for further research applications. Statistical analysis revealed that only two factors significantly affected sample quality. First, the extent of MRI-derived necrosis was significantly higher in unsuitable samples (mean 18.0 %) than in suitable samples (mean 8.3 %) (p = 0.0273). Second, prior treatment with target-specific therapeutics (TST) was associated with a lower proportion of suitable samples (47 %) compared to no prior TST (79 %) (p = 0.018). Logistic regression confirmed these variables as significant predictors, with MRI-derived necrosis (odds ratio 1.049) and target-specific therapy exposure (odds ratio 4.486) independently increasing the likelihood of obtaining suboptimal samples. Other parameters, including age, gender, metastasis volume, localization, primary cancer site, and other therapeutic interventions, showed no significant impact on sample quality. Based on these findings, the collection pipeline was modified to include evaluation by board-certified neuropathologists before samples are used for research purposes, improving the efficiency of translational research utilizing brain metastasis tissue.
{"title":"Impact of preoperative clinical patient parameters on surgically obtained brain metastasis samples for translational research","authors":"Adrian Rombach , Maximilian Geissler , Liu Xiao , Lina-Elisabeth Qasem , Lena Stange , Vincent Prinz , Daniel Jussen , Somaya Landolsi , Konstantinos D. Kokkaliaris , Hind Medyouf , Lisa Sevenich , Pia Zeiner , Yvonne Reiss , Pinar Cakmak , Moritz Armbrust , Katharina J. Weber , Karl Heinz Plate , Stefan Offermanns , Thomas Broggini , Marcus Czabanka","doi":"10.1016/j.mcp.2025.102055","DOIUrl":"10.1016/j.mcp.2025.102055","url":null,"abstract":"<div><div>Human tissue samples are a crucial resource for cancer research, offering key insights into physiological and pathological processes while enabling comprehensive characterization of molecular signatures across cancer subtypes. Recent advances in genetic analysis techniques lead to a substantiall expansion of specific molecular pathways knowledge. The application of these technologies to fresh tissue samples from patients undergoing surgical resection for metastatic disease represents a promising approach to gain a deeper understanding of the biology of brain metastasis. Brain metastases remain particularly challenging due to their poor prognosis and the complex mechanisms underlying central nervous system invasion. This study sought to identify preoperative factors influencing the research utility of fresh brain metastasis tissue samples. A pipeline was established to transfer fresh, surplus tissue from surgical resections to research laboratories with histological quality assessment. Of the fifty-five fresh specimens collected, thirty-eight (69 %) were classified as suitable for further research applications. Statistical analysis revealed that only two factors significantly affected sample quality. First, the extent of MRI-derived necrosis was significantly higher in unsuitable samples (mean 18.0 %) than in suitable samples (mean 8.3 %) (p = 0.0273). Second, prior treatment with target-specific therapeutics (TST) was associated with a lower proportion of suitable samples (47 %) compared to no prior TST (79 %) (p = 0.018). Logistic regression confirmed these variables as significant predictors, with MRI-derived necrosis (odds ratio 1.049) and target-specific therapy exposure (odds ratio 4.486) independently increasing the likelihood of obtaining suboptimal samples. Other parameters, including age, gender, metastasis volume, localization, primary cancer site, and other therapeutic interventions, showed no significant impact on sample quality. Based on these findings, the collection pipeline was modified to include evaluation by board-certified neuropathologists before samples are used for research purposes, improving the efficiency of translational research utilizing brain metastasis tissue.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"84 ","pages":"Article 102055"},"PeriodicalIF":3.0,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145460548","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}
Pub Date : 2025-11-01DOI: 10.1016/j.mcp.2025.102054
Su Qin , Jing Zhang , Meifang Cao , Tao Jiang , Baohong Jiang
This study aims to explore the lymphangiogenesis (LG)-related diagnostic markers of abdominal aortic aneurysm (AAA) through bioinformatics, as well as the alteration of the regional lymphatic system during the progression of AAA and the influence of lymphatic drainage obstruction on AAA progression. 2957 differentially expressed genes (DEGs) were identified between the AAA patient group and the healthy donor group in Gene Expression Omnibus microarray datasets. Subsequently, the DEGs and the LG gene were intersected, and 93 genes were obtained. Weighted gene co-expression network analysis (WGCNA) was performed to obtain module genes. Module genes intersected with the above 93 genes, and 26 genes were obtained. Five hub genes (HSPA5, RAB10, RAB1A, RAF1, SMAD4) identified by machine learning may serve as diagnostic candidates for AAA patients through nomogram and ROC evaluation. Gene set enrichment analysis (GSEA) and immune infiltration analysis were performed further to understand the function of these candidate genes and explore the effect of immunity in AAA, respectively. By establishing an AAA animal model, it was found that the iliac lymph nodes around the abdominal aorta were significantly enlarged, and the number and lumen size of lymphatic vessels in the vessel wall were both significantly increased during the progression of AAA. Additionally, AAA was significantly promoted by ligating lymphatic vessels, which caused lymphatic drainage obstruction around the abdominal aorta. Our findings have the potential to enhance knowledge about the development and diagnosis of AAA.
本研究旨在通过生物信息学的方法探讨腹主动脉瘤（AAA）的淋巴管生成（LG）相关诊断指标，以及AAA进展过程中局部淋巴系统的改变及淋巴引流阻塞对AAA进展的影响。在基因表达集成芯片（Gene Expression Omnibus microarray）数据集中，鉴定出AAA患者组与健康供者组之间存在2957个差异表达基因。随后，将DEGs与LG基因进行交叉，得到93个基因。采用加权基因共表达网络分析（WGCNA）获得模块基因。模块基因与上述93个基因相交，得到26个基因。通过机器学习识别的5个中心基因（HSPA5、RAB10、RAB1A、RAF1、SMAD4）可通过nomogram和ROC评价作为AAA患者的候选诊断基因。进一步进行基因集富集分析（GSEA）和免疫浸润分析，分别了解这些候选基因的功能，探讨免疫在AAA中的作用。通过建立AAA动物模型发现，在AAA的进展过程中，腹主动脉周围的髂淋巴结明显增大，血管壁淋巴管数量和管腔大小均明显增加，结扎淋巴管可明显促进AAA，造成腹主动脉周围淋巴管引流阻塞。我们的发现有可能提高对AAA的发展和诊断的认识。
{"title":"Identification of lymphangiogenesis-related diagnostic model for predicting abdominal aortic aneurysm onset and progression and validation of lymphopoiesis in abdominal aortic aneurysm","authors":"Su Qin , Jing Zhang , Meifang Cao , Tao Jiang , Baohong Jiang","doi":"10.1016/j.mcp.2025.102054","DOIUrl":"10.1016/j.mcp.2025.102054","url":null,"abstract":"<div><div>This study aims to explore the lymphangiogenesis (LG)-related diagnostic markers of abdominal aortic aneurysm (AAA) through bioinformatics, as well as the alteration of the regional lymphatic system during the progression of AAA and the influence of lymphatic drainage obstruction on AAA progression. 2957 differentially expressed genes (DEGs) were identified between the AAA patient group and the healthy donor group in Gene Expression Omnibus microarray datasets. Subsequently, the DEGs and the LG gene were intersected, and 93 genes were obtained. Weighted gene co-expression network analysis (WGCNA) was performed to obtain module genes. Module genes intersected with the above 93 genes, and 26 genes were obtained. Five hub genes (HSPA5, RAB10, RAB1A, RAF1, SMAD4) identified by machine learning may serve as diagnostic candidates for AAA patients through nomogram and ROC evaluation. Gene set enrichment analysis (GSEA) and immune infiltration analysis were performed further to understand the function of these candidate genes and explore the effect of immunity in AAA, respectively. By establishing an AAA animal model, it was found that the iliac lymph nodes around the abdominal aorta were significantly enlarged, and the number and lumen size of lymphatic vessels in the vessel wall were both significantly increased during the progression of AAA. Additionally, AAA was significantly promoted by ligating lymphatic vessels, which caused lymphatic drainage obstruction around the abdominal aorta. Our findings have the potential to enhance knowledge about the development and diagnosis of AAA.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"85 ","pages":"Article 102054"},"PeriodicalIF":3.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145439965","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}
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