{"title":"Adjuvant Chemotherapy Necessity in Stage I Ovarian Endometrioid Carcinoma: A SEER-Based Study Verified by Single-Center Data and Meta-Analysis.","authors":"Liang Yu, Mingrui Zhao, Jinhui Liu, Yuqin Yang, Lin Zhang, Wenjun Cheng","doi":"10.32604/or.2025.065137","DOIUrl":"10.32604/or.2025.065137","url":null,"abstract":"<p><strong>Background: </strong>The benefit of adjuvant chemotherapy for stage I ovarian endometrioid carcinoma (OEC) remains controversial. Hence, the study sought to explore its value in stage I OEC patients.</p><p><strong>Methods: </strong>Stage I OEC patients (1988-2018) were identified from the Surveillance, Epidemiology, and End Results (SEER) database. Multivariate Cox analysis was used to control confounders. Logistic regression was used to explore factors associated with adjuvant chemotherapy. Cox regression analysis and Kaplan-Meier curves were used to assess the survival benefits. Single-center clinical data and meta-analysis following PRISMA guidelines provided external validation.</p><p><strong>Result: </strong>Adjuvant chemotherapy correlated with improved survival (Hazard Ratio (HR): 0.860, <i>p</i> = 0.011), as did lymphadenectomy (HR: 0.842, <i>p</i> < 0.001). Higher age, pathological stage, and tumor grade negatively affected survival. Chemotherapy administration associated with higher pathological stage (IB: Odds Ratio (OR) 1.565, <i>p</i> < 0.001; IC: OR 4.091, <i>p</i> < 0.001), higher grade (G2: OR 2.336, <i>p</i> < 0.001; G3: OR 4.563, <i>p</i> < 0.001), and lymphadenectomy (OR 1.148, <i>p</i> = 0.040). Stratification analysis showed adjuvant chemotherapy failed to improve prognosis in stage IA/IB patients regardless of grade or lymphadenectomy. For stage IC patients, chemotherapy benefited grade 1-2 or grade 3 patients without lymphadenectomy, and grade 3 patients with lymphadenectomy. Meta-analysis revealed reduced recurrence in stage IC patients (OR = 0.50, <i>p</i> = 0.035).</p><p><strong>Conclusion: </strong>Adjuvant chemotherapy confers survival benefits for stage IC patients, particularly those without lymphadenectomy.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"3007-3022"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12493988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233034","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}
Oncology ResearchPub Date : 2025-09-26eCollection Date: 2025-01-01DOI: 10.32604/or.2025.067666
Yuhan Xie, Shaden A M Khalifa, Hesham R El-Seedi, Paolo Coghi
{"title":"Multi-Target Biological Activities of Podophyllotoxin-Derived Natural Products.","authors":"Yuhan Xie, Shaden A M Khalifa, Hesham R El-Seedi, Paolo Coghi","doi":"10.32604/or.2025.067666","DOIUrl":"10.32604/or.2025.067666","url":null,"abstract":"<p><p>Podophyllotoxin is a well-studied natural product. Because of its unique structure and ability to inhibit cancer cells, it has been changed in different ways to find out its pharmacological properties. This paper discusses the common chemical modifications of podophyllotoxin molecules, including the C-4 and E-4 site replacements. Furthermore, its common inhibitory effects on cancer cells and antiparasitic activities, among others, are outlined by the connection between conformational changes and pharmacological activities. Importantly, Podophyllotoxin can effectively overcome the phenomenon of multidrug resistance through a dual-targeting mechanism, including inhibition of microtubule protein synthesis and topoisomerase II activity, and induces cell cycle arrest and apoptosis. Recent findings reveal its potential to modulate immune responses through the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, further extending beyond its classical mechanisms. This study finally provides a systematic summary of the activity of podophyllotoxin in common cancer cells, including those in the breast, lung, and prostate.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2673-2697"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233088","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}
Oncology ResearchPub Date : 2025-09-26eCollection Date: 2025-01-01DOI: 10.32604/or.2025.066260
Rosa Scarpitta, Emiliano Cappello, Alice Cangialosi, Veronica Gori, Giulia De Luca, Giovanni Gori, Guido Bocci
{"title":"Pharmacological Phase I Clinical Trials in Pediatric Brain Tumors (1990-2024): A Historical Perspective.","authors":"Rosa Scarpitta, Emiliano Cappello, Alice Cangialosi, Veronica Gori, Giulia De Luca, Giovanni Gori, Guido Bocci","doi":"10.32604/or.2025.066260","DOIUrl":"10.32604/or.2025.066260","url":null,"abstract":"<p><p>Central nervous system (CNS) tumors are the most common solid tumors in pediatric patients and the leading cause of childhood cancer-related mortality. Their rarity compared to adult cancers has made enrolling sufficient cases for clinical trials challenging. Consequently, pediatric CNS tumors were long treated with adult protocols despite distinct biological and clinical characteristics. This review examines key aspects of phase I pediatric oncology trials, including study design, primary outcomes, and pharmacological approaches, along with secondary considerations like clinical responses and ethical aspects. Firstly, we evaluated all phase I trial protocols focusing on pediatric CNS tumors with accessible results published in scientific databases (Pubmed, Scopus, Embase, Web of Science, and Google Scholar) from 1990 to November 2024. Secondly, we searched EudraCT and ClinicalTrials.gov on 30 November 2024 for ongoing trials. Our search yielded 60 completed phase I studies and 15 trials in progress. Dividing them by chronological order revealed that study designs and the response assessments evolved as the understanding of CNS tumor biology increased. Despite advancements improving diagnosis, management, and prognostication, mortality remains high, and morbidity persists. Notably, pediatric pharmacokinetics and pharmacodynamics differ from adults, complicating trial comparisons and dosage optimization. Future efforts should focus on large-scale clinical data collection to enhance trial efficiency.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2603-2656"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233188","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}
Oncology ResearchPub Date : 2025-09-26eCollection Date: 2025-01-01DOI: 10.32604/or.2025.066624
Neha Raina, Radha Rani, Mahika Kanojia, Avril Mathias, Keshav Raj Paudel, Ashish Garg, Hardeep Singh Tuli, A T M Mijanur Rahman, Vetriselvan Subramaniyan, Madhu Gupta
{"title":"Nanotechnology-Driven Treatment Strategies for Breast Cancer: Recent Advances and Innovations.","authors":"Neha Raina, Radha Rani, Mahika Kanojia, Avril Mathias, Keshav Raj Paudel, Ashish Garg, Hardeep Singh Tuli, A T M Mijanur Rahman, Vetriselvan Subramaniyan, Madhu Gupta","doi":"10.32604/or.2025.066624","DOIUrl":"10.32604/or.2025.066624","url":null,"abstract":"<p><p>Breast cancer is among the most prevalent cancers in females globally and has the highest mortality rate. The emergence of pharmacologic resistance in breast cancer is a significant challenge for researchers in the pursuit of effective treatment. Investigations in cancer nanotechnology have been transformed by the advancement of smart polymers, lipids, and inorganic materials. Research is now being conducted in the field of innovative nano-pharmaceutical formulations aimed at enhancing the efficacy and durability of chemotherapy. Nanotechnology-based delivery systems are beneficial for combating breast cancer due to theranostic applications, augmented drug encapsulation, decreased degradation, and minimal adverse effects. This review discusses breast cancer and its stages, various risk factors, and pathogenesis, in addition to diagnosis and treatment. Novel nanocarriers are included with the most recent findings in this area and the potential use of these nanocarriers in cancer therapy that centers on their clinical usage for improved treatment. Patents and promising clinical trial results are also explained in detail, with nanotoxicity, ethical concerns, and regulations. This study underscores the importance of treatment strategies using nanotechnology, highlighting the advancing paradigm of breast cancer care. This article examines the prospects, obstacles, and future trajectories of nanomedicines.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2787-2831"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233206","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":"Predictive Value of Serum VEGF Levels in Non-Small Cell Lung Cancer: A Review.","authors":"Eleni Kokkotou, Andriani Charpidou, Nikolaos Syrigos","doi":"10.32604/or.2025.066228","DOIUrl":"10.32604/or.2025.066228","url":null,"abstract":"<p><p>Vascular endothelial growth factor (VEGF) and its receptors (VEGFRs) serve an essential role in tumor angiogenesis and have emerged as potential therapeutic targets in lung cancer. This review explores the significance of serum VEGF levels as a predictive biomarker in non-small cell lung cancer (NSCLC). The VEGF family, consisting of VEGFA, VEGFB, VEGFC, VEGFD, and placenta growth factor (PlGF), engages with specific receptors, including tyrosine kinase receptors (VEGFR-1, VEGFR-2, and VEGFR-3) and neuropilin receptors (NRP-1 and NRP-2), to promote angiogenesis and lymphangiogenesis. VEGF-A, the primary component of the VEGF family, binds to VEGFR-2 to stimulate endothelial cell proliferation and migration, while VEGF-B, VEGF-C, and VEGF-D interact with VEGFR-1 and VEGFR-3 to regulate tumor angiogenesis, lymphangiogenesis, and metastasis. The VEGF/VEGFR signaling pathway activates various downstream effectors, including phospholipase Cγ1, mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), which are essential for maintaining vascular homeostasis and promoting angiogenesis. In NSCLC, elevated serum VEGF levels have been observed, and the VEGF/VEGFR axis is frequently impaired, leading to irregular blood vessel formation and metastatic spread. Despite the development of anti-VEGF therapies, their impact on lung cancer outcomes has been limited. Further research is needed to optimize the effectiveness of these treatments and elucidate the potential of serum VEGF as a predictive biomarker in NSCLC.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2657-2672"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233155","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":"SARS-CoV-2 Vaccine-Induced Seroconversion and Immune Correlates in Patients with Hematological Malignancies. A Real World Study.","authors":"Norbert Nass, Mohamad-Kamal Yaakoub, Alexandra-Victorita Simion, Hartmut Kroll, Sabine Westphal, Judith Pannier, Gerhard Behre","doi":"10.32604/or.2025.067561","DOIUrl":"10.32604/or.2025.067561","url":null,"abstract":"<p><strong>Background: </strong>Patients with hemato-oncological malignancies may respond insufficiently to vaccination, especially in terms of antibody titer. The antibody response depends on the type of malignancy as well as the type and timing of treatment. We intended to evaluate this using real-world data from patients of our regional hospital. This study also considers the role of immune status, including T-cell activation markers, in predicting vaccination success.</p><p><strong>Methods: </strong>Seventeen patients of our hospital having a hematological malignancy were included in this study, including myeloma, lymphoma, as well as acute myeloid leukemia (AML) and chronic lymphoid leukemia (CLL). All patients were vaccinated against Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) using Tozinameran following current recommendations. Circulating antibodies directed against the spike protein of SARS-CoV-2 were determined by a commercial immune assay. Immune status was determined from peripheral blood by flow cytometry. Both parameters were followed in fifteen patients who provided sufficient follow-up data for up to one year. Patients were categorized as responders or non-responders, and differences in diagnosis, treatment, and immune status were analyzed.</p><p><strong>Results: </strong>Antibody response depended on both diagnosis and treatment. Active treatment directed against B-cells, such as anti-Cluster of Differentiation 20 (CD20) therapy, was associated with weak seroconversion. For CD38-as well as proteasome-directed therapies, the data suggest that responders as well as non-responders exist. Notably, low peripheral B-cell numbers and high CD3+HLADR+cell counts correlated with weak seroconversion upon vaccination.</p><p><strong>Conclusions: </strong>We suggest that peripheral immune status can be applied as a predictive biomarker for seroconversion upon vaccinations.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2923-2935"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233162","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}
Oncology ResearchPub Date : 2025-09-26eCollection Date: 2025-01-01DOI: 10.32604/or.2025.063644
Lang Chen, Rui Dong, Xuan Huan
{"title":"Deubiquitinating Enzyme OTUDs: Focus on Cancers and Antiviral Response.","authors":"Lang Chen, Rui Dong, Xuan Huan","doi":"10.32604/or.2025.063644","DOIUrl":"10.32604/or.2025.063644","url":null,"abstract":"<p><p>Deubiquitinating enzymes (DUBs) are key enzymes capable of cleaving ubiquitin chains and synergizing with ubiquitination modifications to regulate the function of key proteins and maintain normal physiological functions. OTUDs are a key subfamily of the ovarian tumor protease (OTU) family, with important DUB activities, and include mainly OTUD1, OTUD2, OTUD3, OTUD4, OTUD5, OTUD6A, and OTUD6B. In recent years, research on OTUD proteins has been gradually emphasized, and their aberrant expression has demonstrated significant research value in many diseases, such as cancer, immune abnormalities, neurological disorders, and embryonic developmental abnormalities. Therefore, a comprehensive understanding of the regulatory mechanisms of OTUD proteins and their use as therapeutic targets for diseases is of great value. This article focuses on the role of individual OTUD proteins in cancer progression and antiviral response. Importantly, in the context of cancer, we elaborate on their deubiquitinated protein targets and summarize the signaling mechanisms by which they promote or inhibit cancer progression. In the future, targeting OTUD proteins may become a therapeutic direction for cancer, and this review may be useful for research related to OTUD proteins and cancer. At present, there is a lack of research on targeted inhibitors or activators of OTUDs. More <i>in vivo</i> and <i>in vitro</i> studies on OTUDs may contribute to the development of inhibitors or agonists targeting OTUDs. Of course, when conducting these studies, researchers also need to pay attention to the impact of OTUDs on the host's antiviral immune response.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2833-2856"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12493990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233049","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}
Oncology ResearchPub Date : 2025-09-26eCollection Date: 2025-01-01DOI: 10.32604/or.2025.067247
Songhua Bei, Qianqian Guo, Xinglei Wu, Fan Li, Yaya Xie, Xiaohong Zhang, Li Feng, Xingxing Zhang
{"title":"<i>HCAR1</i> Modulates Ferroptosis in Gastric Cancer via Lactate-Mediated AMPK-SCD1 Signaling and Lipid Metabolism.","authors":"Songhua Bei, Qianqian Guo, Xinglei Wu, Fan Li, Yaya Xie, Xiaohong Zhang, Li Feng, Xingxing Zhang","doi":"10.32604/or.2025.067247","DOIUrl":"10.32604/or.2025.067247","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis is a type of regulated cell death characterized by iron-dependent lipid peroxidation, which has been linked to tumor progression and therapeutic resistance. However, the contribution of lactate metabolism and its receptor, hydroxycarboxylic acid receptor 1 (HCAR1), in ferroptosis regulation in gastric cancer (GC) remains poorly understood. Focusing specifically on its effects on cell proliferation, ferroptosis regulation, and the disruption of lactate-mediated metabolic pathways, the study aimed to clarify the role of HCAR1 in GC progression.</p><p><strong>Methods: </strong>Bioinformatics analysis identified prognostic genes associated with ferroptosis in GC. Receiver operating characteristic (ROC) curves were generated to assess the diagnostic potential of the predictive genes. The biological role of HCAR1 was investigated through gain and loss-of-function experiments in GC cell lines, followed by assessments of cell viability, oxidative stress indicators, gene/protein expression, and ferroptosis sensitivity under lactate stimulation or HCAR1 modulation.</p><p><strong>Results: </strong>HCAR1 was significantly upregulated in GC tissues and linked to poor patient outcomes. Silencing HCAR1 inhibited GC cell growth and induced ferroptosis, as shown by increased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), along with decreased expression of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4). Conversely, HCAR1 overexpression or exposure to extracellular lactate inhibited ferroptosis and activated antioxidant defenses. Mechanistically, lactate activation of HCAR1 increases ATP levels, which in turn inactivates AMP-activated protein kinase (AMPK). It also upregulates stearoyl-CoA desaturase 1 (SCD1) through the sterol regulatory element binding protein 1 (SREBP1) signaling pathway. Blocking HCAR1 reversed these effects and restored ferroptosis sensitivity.</p><p><strong>Conclusion: </strong>HCAR1 mediates lactate-driven ferroptosis resistance in GC through the AMPK-SCD1 signaling pathway. Targeting the HCAR1-lactate axis may offer a promising strategy for overcoming metabolic adaptation and improving GC treatment outcomes.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"3101-3125"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233084","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}
Oncology ResearchPub Date : 2025-09-26eCollection Date: 2025-01-01DOI: 10.32604/or.2025.065380
Jianwei Wang, Xinzhi Yang, Lvbiao Lin, Jianbo Yu, Jie Mao
{"title":"Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation.","authors":"Jianwei Wang, Xinzhi Yang, Lvbiao Lin, Jianbo Yu, Jie Mao","doi":"10.32604/or.2025.065380","DOIUrl":"10.32604/or.2025.065380","url":null,"abstract":"<p><strong>Objectives: </strong>Glioma, as the most lethal primary brain malignancy with poor prognosis, requires further elucidation on the functional role of long noncoding RNA (lncRNA) DDX11 antisense RNA 1 (DDX11-AS1) in its pathogenesis, despite its established oncogenic functions in other cancers. Therefore, this study sought to characterize the oncogenic role and molecular mechanism of DDX11-AS1 in glioma.</p><p><strong>Methods: </strong>DDX11-AS1 expression levels were analyzed in clinical surgical glioma specimens and publicly available datasets. The functional roles of DDX11-AS1 on glioma cell proliferation and migration were investigated using <i>in vitro</i> knockdown and overexpression assays. <i>In vivo</i> tumor growth was assessed using orthotopic glioma-bearing mouse models. To elucidate the regulatory axis involving DDX11-AS1, miR-1183, and E2F transcription factor 7 (E2F7), we performed competitive endogenous RNA (ceRNA) analysis and conducted functional rescue experiments via miR-1183 inhibition.</p><p><strong>Results: </strong>DDX11-AS1 expression was markedly upregulated in clinical glioma specimens. Functionally, DDX11-AS1 knockdown significantly suppressed glioma cell proliferation and migration <i>in vitro</i>, while its overexpression exacerbated these malignant phenotypes. Orthotopic glioma-bearing mouse models confirmed that DDX11-AS1 drives <i>in vivo</i> glioma tumor growth. Mechanistically, DDX11-AS1 functions as a ceRNA by competitively interacting with miR-1183. Critically, inhibition of miR-1183 rescued the suppressive effects of DDX11-AS1 knockdown on glioma tumorigenic phenotypes and restored E2F7 expression levels.</p><p><strong>Conclusions: </strong>This study demonstrates that lncRNA DDX11-AS1 promotes glioma progression by regulating the miR-1183/E2F7 axis, indicating a potential therapeutic target for glioma.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"3023-3040"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233080","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}