Translational cancer research最新文献

{"title":"SERPINH1, a regulatory factor of oligodendroglioma cell invasion and extracellular matrix secretion, as a novel prognostic biomarker and therapeutic target.","authors":"Xue Chen, Shunyao Li, Huijuan Zhao, Lan Deng, Liyun Zhong","doi":"10.21037/tcr-2025-2106","DOIUrl":"https://doi.org/10.21037/tcr-2025-2106","url":null,"abstract":"<p><strong>Background: </strong>Oligodendroglioma is a specific type of brain glioma, and relatively little research has been conducted on it. The expression and prognosis of serine protease peptidase inhibitor, branch H, member 1 (SERPINH1) in some malignant tumors have been studied, but the prognosis value and potential mechanism of this gene in oligodendroglioma have not been reported yet, and further research is needed. This study aims to reveal the expression characteristics and biological functions of SERPINH1 in oligodendroglioma cells, laying the foundation for targeted drug development.</p><p><strong>Methods: </strong>Retrospective RNA sequencing (RNA-seq) data analysis was conducted in a cohort of 171 patients with oligodendroglioma in the Chinese Glioma Genome Atlas (CGGA) database and 149 patients in The Cancer Genome Atlas (TCGA) database. In addition, we used Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Kaplan-Meier analyses, univariate and multivariate Cox regression analyses, correlation analysis, as well as Kolmogorov-Smirnov test and Unpaired <i>t</i>-test.</p><p><strong>Results: </strong>SERPINH1 is highly enriched in short-lived patients compared to long-lived oligodendroglioma patients. SERPINH1 is relatively highly expressed in more malignant oligodendrogliomas. Functional enrichment shows that SERPINH1 is closely related to the tumor invasion function of oligodendroglioma. Further research has confirmed that SERPINH1 promotes the invasive function of tumor cells by regulating the secretion of extracellular matrix. Prognostic analysis shows that SERPINH1 is an independent poor prognostic factor for oligodendroglioma.</p><p><strong>Conclusions: </strong>We found that SERPINH1 can serve as an independent prognostic biomarker for oligodendroglioma. It may be a potential new target for the treatment of oligodendroglioma.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"198"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated bulk RNA-seq and scRNA-seq identification of a novel \"PET-<i>SPI1</i>-<i>MYL9</i>\" transcriptional axis in lung adenocarcinoma driven by polyethylene terephthalate exposure.","authors":"Qian Su, Juanjuan Guo, Yilin Gu, Wang Xu, Haihong Cao, Yongbin Lu, Fei Su, Xiaoming Hou, Tao Zhang","doi":"10.21037/tcr-2025-1-2630","DOIUrl":"https://doi.org/10.21037/tcr-2025-1-2630","url":null,"abstract":"<p><strong>Background: </strong>Airborne microplastic polyethylene terephthalate (PET) accumulates in human lungs and is linked to respiratory pathologies; however, its molecular role in lung adenocarcinoma (LUAD) remains unclear. This study aims to explore the potential carcinogenic mechanisms of PET exposure in LUAD.</p><p><strong>Methods: </strong>We integrated single-cell RNA sequencing, machine learning algorithms [including Classification and Regression Trees (CART), Naïve Bayes (NB), random forest (RF), and support vector machine (SVM)], molecular docking, survival analysis, and multi-omics data. Through differential expression screening across datasets combined with Venn analysis, we identified seven PET-associated oncogenic targets. Seven PET-associated oncogenic targets were identified via differential gene screening and Venn analysis.</p><p><strong>Results: </strong><i>MYL9</i> was validated as a downregulated, LUAD-protective biomarker associated with significant survival benefit [hazard ratio (HR) =0.59, 0.16, 0.23; all P<0.05]. These findings were consistent across the Human Protein Atlas (HPA) database, co-expression networks, and three independent LUAD datasets. <i>SPI1</i> was identified as a key transcriptional regulator, showing strong co-expression with <i>MYL9</i> (R=0.556, P<0.05) and concurrent downregulation in LUAD. Molecular docking revealed that PET bound to the DNA-binding pocket of SPI1 (ΔG =-5.30 kcal·mol-1), suggesting its transcriptional inhibition of <i>MYL9</i>.</p><p><strong>Conclusions: </strong>Our integrated bioinformatics approach supports a novel \"PET-<i>SPI1</i>-<i>MYL9</i>\" transcriptional axis, revealing a potential non-genotoxic carcinogenic pathway for PET. While the computational evidence is robust, further wet-lab experiments are needed to validate the binding and transcriptional inhibition mechanism. This model provides a framework for understanding airborne microplastic toxicity in LUAD. We propose that PET promotes LUAD by disrupting the <i>SPI1</i>-<i>MYL9</i> transcriptional axis, highlighting a potential environmental trigger and candidate targets for diagnostic and therapeutic strategies.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"173"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New model for remote symptom management and self-care of cancer patients based on digital health platforms: a narrative review.","authors":"Wen Chen, Yue Deng, Di Zhu, Huan Zhu","doi":"10.21037/tcr-2025-1-2621","DOIUrl":"https://doi.org/10.21037/tcr-2025-1-2621","url":null,"abstract":"<p><strong>Background and objective: </strong>With the increasing global cancer burden and prolonged survival of patients, effective post-treatment symptom management and self-care have become essential components of chronic cancer care. Traditional follow-up-based medical models often fail to capture dynamic symptom fluctuations, leading to suboptimal adherence and increased healthcare utilization. The emergence of digital health platforms provides new opportunities for remote symptom monitoring (RSM) and patient-centered care. This narrative review aimed to synthesize recent global evidence on the use of digital health platforms for remote symptom management and self-care among cancer patients, focusing on their technological frameworks, clinical benefits, and implementation challenges.</p><p><strong>Methods: </strong>A structured literature search was conducted across PubMed, Web of Science, Embase, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Institute of Electrical and Electronics Engineers (IEEE) Xplore for studies published in English between January 2018 and December 2024. The search combined controlled vocabulary and free-text terms related to digital health platforms, cancer, symptom management, and self-care. Reference lists of included studies were also manually screened. Eligible studies included those involving cancer patients and evaluating digital health interventions for RSM or self-management.</p><p><strong>Key content and findings: </strong>The reviewed studies covered diverse digital health platforms integrating wearable sensors, mobile applications, and cloud-based analytics for real-time symptom tracking and personalized interventions. Core functional modules commonly identified included symptom monitoring, patient education, and psychosocial support. Evidence suggested that these platforms enhance patient empowerment, improve communication between patients and clinicians, and support proactive care through early detection of symptom exacerbations. However, significant barriers remain, including issues of data privacy and security, regulatory heterogeneity, and the digital devices that may limit equitable access.</p><p><strong>Conclusions: </strong>Digital health platforms are transforming oncology care from a physician-centered model to a collaborative, technology-enabled framework that supports continuous, patient-driven symptom management. While existing evidence demonstrates their feasibility and clinical benefits, future research should emphasize standardization, long-term clinical validation, and culturally adaptable implementation models. Addressing these priorities may enhance both patient quality of life and the efficiency of healthcare resource utilization in cancer survivorship care.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"217"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triglyceride-to-glucose index and lymphocyte-to-monocyte ratio enhance prognostic accuracy for colorectal cancer patients: a multicenter machine learning cohort study.","authors":"Lei Liang, Yahan Zhang, Xinyu He, Tawfik Ali Hamood Alburiahi, Zhiyong Kou, Jun Yang, Jianhua Zhang, Yang Zhang, Chengxun Jiang, Weiqing Liu","doi":"10.21037/tcr-2025-1-2893","DOIUrl":"https://doi.org/10.21037/tcr-2025-1-2893","url":null,"abstract":"<p><strong>Background: </strong>Triglyceride-to-glucose index (TyG), a key diagnostic marker for insulin resistance, has been linked to colorectal cancer (CRC). Nevertheless, TyG prognostic significance in CRC survival has not been established. This study seeks to develop and validate a robust machine learning (ML) based predictive model combining TyG and inflammatory markers for predicting long-term survival outcomes in CRC patients.</p><p><strong>Methods: </strong>A retrospective study was performed on (n=1,893) CRC patients who underwent radical surgery at The First Affiliated Hospital of Kunming Medical University. The patients were randomly assigned to training cohort (70%) and an internal validation cohort (30%). An external validation cohort (n=493) from another hospital was used to test model generalizability. Independent prognostic factors were identified via multivariate Cox regression. An integrative predictive model was constructed using various ML algorithms [random survival forest (RSF), eXtreme Gradient Boosting (XGBoost), gradient boosting machines (GBM)], evaluated by concordance index (C-index), receiver operating characteristic (ROC) curve, calibration plots, and decision curve analyses (DCAs).</p><p><strong>Results: </strong>The final model integrated eight independent prognostic factors: age, lymphocyte-to-monocyte ratio (LMR), TyG, carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA199), Union for International Cancer Control (UICC) stage, tumor differentiation, and perineural invasion. The model achieved good predictive accuracy (C-index: training =0.742, internal validation =0.735, external validation =0.752). ROC curves demonstrated robust predictive accuracy for 1-, 3-, and 5-year survival [area under the curve (AUC): 0.79, 0.76, 0.74, respectively]. SHapley Additive exPlanations (SHAP) analysis ranked TyG as the second-most influential prognostic indicator.</p><p><strong>Conclusions: </strong>Elevated TyG index independently predicts favorable long-term outcomes in CRC patients. Our validated ML model, combining TyG, inflammatory markers, and clinicopathological features, provides a reliable, economical, and practical clinical tool for prognosis assessment. Further multicenter, prospective studies are necessary to confirm the widespread applicability of this model.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"199"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"m6A modified circPTK2 mediates TNBC chemotherapy resistance.","authors":"Jinyang Yuan, Bin Xie, Xiaoqian Wen, Ge Zhao, Honghong Shen","doi":"10.21037/tcr-2025-1-2634","DOIUrl":"https://doi.org/10.21037/tcr-2025-1-2634","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Circular RNAs (circRNAs) act as novel biomarkers associated with drug resistance in triple-negative breast cancer (TNBC). Our previous study has demonstrated that the Wnt/β-catenin pathway mediates TNBC chemoresistance, and the present study further investigates its upstream regulatory mechanisms.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Gene chip analysis was used to screen for circRNAs in drug-resistant cells. The expression levels of circPTK2 in cells and tissues were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8), Transwell, flow cytometry, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL), three-dimensional (3D) multicellular tumor spheroid culture model, 5-ethynyl-2'-deoxyuridine (EdU) proliferation staining, western blot and immunofluorescence were used to detect the influence of circPTK2 on the drug sensitivity, cell invasion, proliferation, apoptosis and DNA damage repair of TNBC cells. The pull-down and dual-luciferase reporter gene assays were used to determine the interaction between circPTK2 and miR-495. Dual luciferase reporter gene assay and RNA immunoprecipitation (RIP) experiment verified the binding of miR-495 to β-catenin. A transplanted tumor model was established in nude mice to determine circPTK2 effects on the chemosensitivity of drug-resistant cells to cisplatin (DDP). Methylated RNA immunoprecipitation (MeRIP) and RNA electrophoretic mobility shift assay (RNA-EMSA) verified the enrichment of the N6-methyladenosine (m6A) methylated region of circPTK2. The m6A quantitative kit was used to detect the level of m6A modification. MeRIP-PCR was used to detect the enrichment amount of m6A-modified circPTK2 (m6A&lt;sup&gt;+&lt;/sup&gt; circPTK2).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;qRT-PCR results indicated that the expression level of circPTK2 in drug-resistant cells was higher than that in parental cells. The expression level of circPTK2 in DDP-resistant tissues was significantly higher than that in DDP-sensitive tissues. circPTK2 has the characteristics of resisting Rnase R digestion and having stronger stability than linear RNA. Knocking down of circPTK2 can reduce the viability and invasion ability of TNBC DDP-resistant cells, promote the DNA damage induced by DDP, and enhance the sensitivity of TNBC cells to DDP. RNA fluorescence in situ hybridization (RNA FISH) results showed that circPTK2 and miR-495 were co-localized in the cytoplasm. The dual luciferase reporter gene activity assay showed the targeted binding of miR-495 to the 3'UTR region of β-catenin. The RNA immunoprecipitation-polymerase chain reaction (RIP-PCR) experiment confirmed that YTH domain-containing protein 1 (YTHDC1) could bind to circPTK2. m6A quantitative kit showed that the m6A modification in the resistant cells was higher than that in the parental cells. qRT-PCR and Western blot results showed that the mRNA and protein expression level of YTHDC1 in the DDP resis","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"162"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13066988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Programmed cell death receptor 1 inhibitors combined with paclitaxel-platinum induction chemotherapy for treating patients with locally advanced nasopharyngeal carcinoma: a real-world retrospective study.","authors":"Lilan Chen, Xing Song, Junjun Chen, Junchao Huang, Wendong Gu, Wenjie Jiang","doi":"10.21037/tcr-2026-1-0029","DOIUrl":"https://doi.org/10.21037/tcr-2026-1-0029","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Concurrent chemoradiotherapy (CCRT) combined with induction chemotherapy (IC) is the standard first-line treatment for locally advanced nasopharyngeal carcinoma (LA-NPC). However, treatment-related toxicities and the risk of recurrence or metastasis remain clinical challenges, which have prompted the development of strategies that can improve efficacy while minimizing adverse effects. The integration of programmed cell death receptor 1 (PD-1) inhibitors with IC has demonstrated significant survival benefits in pivotal phase III trials. This study aimed to assess the efficacy and safety of PD-1 inhibitors combined with IC consisting of a paclitaxel-platinum (TP) regimen for LA-NPC in a real-world clinical setting.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This retrospective study enrolled patients diagnosed with stage III or IVA NPC who received treatment between January 2021 and December 2024. Clinical records and radiographic data were systematically reviewed. Based on the administration of PD-1 inhibitor immunotherapy during IC, patients were categorized into a control group and an immunotherapy group. Propensity score matching (PSM) was performed sequentially after IC and again after CCRT to minimize confounding factors. Matching was based on clinically relevant covariates, including age, gender, differentiation, tumor-node-metastasis stage, Epstein-Barr virus DNA level and treatment cycle. Between-group differences in treatment response and adverse events were assessed via Chi-squared tests for categorical variables. The primary endpoint is the disease control rate (DCR) after IC. The secondary endpoints include the objective response rate (ORR) after CCRT, the incidence of adverse events, and their severity.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;A total of 150 patients with LA-NPC were included, among whom 76 received standard IC, and 74 received combined immunotherapy. In the PSM analysis, 54 patients were matched to each group, and the immunotherapy group demonstrated significantly higher disease control during the IC phase (P=0.004), with a partial response (PR) rate of 94.4% compared to 70.4% in the control group. Following CCRT, 49 patients per group matched by PSM showed no significant differences in complete response (CR) or PR rates (P=0.25). The CR rates were 10.2% and 18.4% in the control group and the immunotherapy group, respectively, while the PR rates were 89.8% and 81.6%, respectively. Furthermore, the groups showed no statistical differences in terms of the incidence of radiotherapy-related adverse events, including oral mucositis (P=0.26), skin reactions (P=0.20), and myelosuppression (P=0.33). No grade 3 or higher immune-related adverse events (irAEs) were reported in the immunotherapy group.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;This real-world study successfully verified that adding PD-1 inhibitors to IC improves early efficacy without increasing toxicity in LA-NPC, providing external validation of key trial","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"210"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147677025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of triphenyl phosphate's pathogenic potential and molecular mechanisms in glioblastoma: an integrated network toxicology investigation employing multiple machine learning approaches.","authors":"Ziyu Wang, Kai Cui, Jialin Wang, Rong Ma, Yanyang Wang","doi":"10.21037/tcr-2025-1-2668","DOIUrl":"https://doi.org/10.21037/tcr-2025-1-2668","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM) is a highly aggressive brain tumor with a poor prognosis, and its etiology involves both genetic and environmental factors. Triphenyl phosphate (TPHP), an organophosphorus flame retardant widely used in various consumer products, has raised public health concerns due to its environmental prevalence and detection in human samples. However, its potential role in GBM pathogenesis remains unclear. This study combined machine learning and molecular simulation docking technology to investigate the effects of TPHP on the pathogenesis and related molecular mechanisms of glioma.</p><p><strong>Methods: </strong>Our study made use of a variety of computational learning methods along with online databases to carry out differential transcriptional expression analysis on different datasets. The aim was to identify target genes related to glioma. Based on the expression levels of key genes, we constructed a risk prediction model. Network toxicology and molecular docking technologies were adopted to investigate how TPHP binds to target proteins.</p><p><strong>Results: </strong>Fourteen genes in total were determined to be potential target genes in relation to TPHP-induced glioma. Further machine learning analysis identified three core target genes (<i>GRM3</i>, <i>IDH2</i>, and <i>DDR2</i>) as key biomarkers for TPHP-induced glioma, and pathway analysis determined the relevant signaling pathways of TPHP. Molecular docking showed that there was a specific binding effect between TPHP and target proteins.</p><p><strong>Conclusions: </strong>It is possible that TPHP influences the pathogenic mechanism of glioma through targeting particular genes and pathways. Results from molecular docking simulations demonstrated a remarkable binding specificity effect between TPHP and target proteins. This effect is highly likely to be the crucial factor contributing to the development of glioma.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"202"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147677049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting chitinase-3-like protein 2 (CHI3L2) suppresses cell proliferation and migration in glioblastoma.","authors":"Zhihong Liu, Dihui Chen, Sijia Liao, Xiuyue Fan, Jiamei Wang, Hongshuang Yue, Huilin Shen, Jijin Wang, Chengning Zhao, Rong Hu, Guangshi Du, Feng Han","doi":"10.21037/tcr-2025-aw-2353","DOIUrl":"https://doi.org/10.21037/tcr-2025-aw-2353","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM), the most common and aggressive subtype of glioma, currently lacks effective therapeutic targets. This study aimed to elucidate the role of chitinase-3-like protein 2 (CHI3L2) and its underlying mechanism in GBM cell proliferation and migration.</p><p><strong>Methods: </strong>Gene Expression Profiling Interactive Analysis 2 (GEPIA2) and Chinese Glioma Genome Atlas (CGGA) databases were used to analyze the messenger RNA (mRNA) expression level of CHI3L2 and its prognostic significance in different grades of glioma patients. Western blotting was performed to determine the protein levels of CHI3L2 in different GBM cell lines. The efficiency of lentivirus-mediated CHI3L2 knockdown or overexpression was tested by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting in LN-229 and U251 cells. Cell proliferation was determined by cell counting kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays. Cell migration was detected by the wound healing assay. Cell cycle distribution was analyzed by flow cytometry. Protein levels of key cell cycle-related regulators (e.g., c-MYC, CDK2, CDK4) and migration-related regulators (e.g., E-cadherin, N-cadherin, MMP2, MMP9) were measured by Western blotting.</p><p><strong>Results: </strong>Integrated bioinformatics analysis demonstrated that high CHI3L2 expression was correlated with shortened overall survival (OS) and disease-free survival (DFS) in GBM patients. CHI3L2 knockdown significantly suppressed cell proliferation, G1/S transition, and cell migration in LN-229 and U251 cells; conversely, CHI3L2 overexpression facilitated these cellular processes. Furthermore, CHI3L2 knockdown markedly reduced the protein levels of c-MYC, CDK2, CDK4, N-cadherin, MMP2, and MMP9 but increased E-cadherin.</p><p><strong>Conclusions: </strong>Elevated CHI3L2 expression drives GBM cell proliferation and migration, suggesting that CHI3L2 is a promising therapeutic target for GBM.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"146"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13066967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative analysis reveals the role of SUMOylation-related patterns in shaping the tumor microenvironment and predicting treatment sensitivity of colorectal cancer.","authors":"Gaojian Cao, Sen Zhang, Hao Zhong, Jie Yu, Xiexiao Cai, Xiangwei Huang, Mengqin Yu, Naijipu Abuduaini, Jingyi Liu, Wanyu Wang, Lih Shyuan Kong, Xiaohan Wang, Bo Feng, Ximo Xu, Qiwen Ye","doi":"10.21037/tcr-2025-aw-2194","DOIUrl":"https://doi.org/10.21037/tcr-2025-aw-2194","url":null,"abstract":"<p><strong>Background: </strong>SUMOylation is a critical post-translational modification that governs protein stability, subcellular localization, and signal transduction. Accumulating evidence suggests that dysregulated SUMOylation contributes to colorectal cancer (CRC) progression. However, its global impact on tumor microenvironment (TME) remodeling and clinical heterogeneity remains incompletely understood. The objective of this study was to establish a robust SUMOylation-related transcriptional signature to quantify SUMOylation activity in CRC and to elucidate its association with immune infiltration patterns, patient prognosis, and therapeutic responsiveness.</p><p><strong>Methods: </strong>Using integrated transcriptomic profiles from The Cancer Genome Atlas (TCGA) and multiple Gene Expression Omnibus (GEO) cohorts (total n=1,226), we systematically curated SUMOylation-related genes (SRGs) and developed a SUMOylation-based scoring system (SUMOscore). Patients were stratified into high and low SUMOscore subgroups, followed by comprehensive evaluation of clinical outcomes, tumor staging, stromal components, and immune-cell infiltration landscapes. Potential responses to immune checkpoint blockade (ICB) and 5-fluorouracil (5-FU) chemotherapy were further inferred using established computational frameworks.</p><p><strong>Results: </strong>Five key SRGs were identified to construct a scoring model that categorizes patients into high and low SUMOscore groups. The SUMOscore is an independent prognostic factor for CRC patients. Higher SUMOscore correlates with shorter overall survival (OS), advanced tumor staging, increased stromal infiltration, and lower tumor mutational burden. Further analysis suggests that CRC patients with lower SUMOscore might be more sensitive to immune checkpoint inhibitors and 5-FU chemotherapy.</p><p><strong>Conclusions: </strong>The SUMOscore captures clinically relevant TME heterogeneity in CRC and may help guide selection of immunotherapy and adjuvant chemotherapy.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"169"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-663a upregulation upon ARID1A depletion promotes the growth and migration of esophageal cancer cells by targeting FKBP8.","authors":"Hongli Liao, Chunyi Ren, Yi Jiang, Fengxiang Wang, Yanyan Dai","doi":"10.21037/tcr-2025-1457","DOIUrl":"https://doi.org/10.21037/tcr-2025-1457","url":null,"abstract":"<p><strong>Background: </strong>ARID1A loss has been shown to promote the development and progression of cancers by modulating different target genes, including microRNAs (miRs). This study was performed to identify ARID1A-regulated miRs involved in esophageal cancer progression.</p><p><strong>Methods: </strong>ARID1A expression in esophageal cancer cell lines was knocked down and the expression of candidate miRs that were differentially expressed between esophageal cancer and adjacent normal tissues was examined. The role of ARID1A-regulated miRs in the growth and migration of esophageal cancer cells was determined.</p><p><strong>Results: </strong><i>ARID1A</i> knockdown caused a significant upregulation of miR-663a in SKGT4 and EC109 esophageal cancer cells. Compared to normal tissues, esophageal cancer samples expressed higher levels of miR-663a. According to the Kaplan-Meier plotter database, high miR-663a expression was significantly associated with poor prognosis in esophageal cancer. Functional studies indicated that miR-663a overexpression promoted the growth, migration, and tumorigenesis of esophageal cancer cells. Silico analysis and dual luciferase reporter assays identified FKBP8 as a target for miR-663a. Knockdown of <i>FKBP8</i> significantly increased the proliferation, colony formation, and migration capacities of esophageal cancer cells. Most importantly, miR-663a-induced aggressive phenotype in esophageal cancer cells relied on the repression of FKBP8 expression.</p><p><strong>Conclusions: </strong>The miR-663a/FKBP8 axis regulated by ARID1A plays a critical role in esophageal cancer cell proliferation and migration and represents a potential therapeutic target for this malignancy.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"15 3","pages":"178"},"PeriodicalIF":1.7,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}