Oncology Research最新文献

{"title":"Igniting Cold Tumors: Multi-Omics-Driven Strategies to Overcome Immune Evasion and Restore Immune Surveillance.","authors":"Xinyao Huang, Renjun Gu, Ziyun Li, Fangyu Wang","doi":"10.32604/or.2025.066805","DOIUrl":"10.32604/or.2025.066805","url":null,"abstract":"<p><p>Cold tumors, defined by insufficient immune cell infiltration and a highly immunosuppressive tumor microenvironment (TME), exhibit limited responsiveness to conventional immunotherapies. This review systematically summarizes the mechanisms of immune evasion and the therapeutic strategies for cold tumors as revealed by multi-omics technologies. By integrating genomic, transcriptomic, proteomic, metabolomic, and spatial multi-omics data, the review elucidates key immune evasion mechanisms, including activation of the WNT/β-catenin pathway, transforming growth factor-β (TGF-β)-mediated immunosuppression, metabolic reprogramming (e.g., lactate accumulation), and aberrant expression of immune checkpoint molecules. Furthermore, this review proposes multi-dimensional therapeutic strategies, such as targeting immunosuppressive pathways (e.g., programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) inhibitors combined with TGF-β blockade), reshaping the TME through chemokine-based therapies, oncolytic viruses, and vascular normalization, and metabolic interventions (e.g., inhibition of lactate dehydrogenase A (LDHA) or glutaminase (GLS)). In addition, personalized neoantigen vaccines and engineered cell therapies (e.g., T cell receptor-engineered T (TCR-T) and natural killer (NK) cells) show promising potential. Emerging evidence also highlights the role of epigenetic regulation (e.g., histone deacetylase (HDAC) inhibitors) and N6-Methyladenosine (m6A) RNA modifications in reversing immune evasion. Despite the promising insights offered by multi-omics integration in guiding precision immunotherapy, challenges remain in clinical translation, including data heterogeneity, target-specific toxicity, and limitations in preclinical models. Future efforts should focus on coupling dynamic multi-omics technologies with intelligent therapeutic design to convert cold tumors into immunologically active (\"hot\") microenvironments, ultimately facilitating breakthroughs in personalized immunotherapy.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2857-2902"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233100","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":"ARPC1B Promotes Clear Cell Renal Cell Carcinoma Progression via the Wnt/β-Catenin Signaling Pathway.","authors":"Jiayin Peng, Yijun Xue, Zhiren Cai, Zhaoguan Li, Kangyan Han, Xiaoqi Lin, Yutong Li, Yumin Zhuo","doi":"10.32604/or.2025.067340","DOIUrl":"10.32604/or.2025.067340","url":null,"abstract":"<p><strong>Background: </strong>Clear cell renal cell carcinoma (ccRCC) is an aggressive malignancy associated with limited treatment options and poor prognosis. Emerging studies suggest that the actin-regulating protein actin-related protein 2/3 complex subunit 1B (ARPC1B), a key regulatory protein within the actin cytoskeleton, could play a pivotal role in ccRCC progression. The current study aimed to uncover the biological functions of ARPC1B and the molecular mechanisms driving its effects in ccRCC.</p><p><strong>Methods: </strong>ARPC1B expression and prognostic implications were analyzed using data sourced from the Gene Expression Profiling Interactive Analysis (GEPIA) platform, immunohistochemical (IHC) staining on 150 tumor samples along with 30 corresponding normal tissues, and Western blotting (WB) analyses across multiple ccRCC-derived cell lines. Functional assays assessing cell proliferation, colony formation capability, migration, invasion, and <i>in vivo</i> tumorigenicity were conducted following either ARPC1B suppression or upregulation. Additionally, WB analysis was utilized to evaluate proteins linked to epithelial-to-mesenchymal transition (EMT) and the Wnt/β-catenin pathway.</p><p><strong>Results: </strong>The findings revealed a substantial elevation of ARPC1B in ccRCC tissues and cell lines, significantly associated with advanced TNM stages, higher Fuhrman grades, and reduced overall survival (OS) (<i>p</i> < 0.001). Multivariate statistical analysis identified ARPC1B as a standalone prognostic factor. Silencing ARPC1B notably impaired ccRCC cellular activities, and tumorigenesis in animal models, whereas augmented ARPC1B expression enhanced these malignant phenotypes. Mechanistically, downregulation of ARPC1B suppressed Wnt/β-catenin signaling and disrupted EMT, indicated by reduced β-catenin, c-Myc, cyclin D1, and ZEB-1 levels, and concurrently increased E-cadherin expression. Additionally, reactivation of the Wnt/β-catenin pathway partly reversed the inhibitory effects of ARPC1B depletion on tumor growth and invasiveness.</p><p><strong>Conclusions: </strong>ARPC1B emerges as an essential oncogenic factor in ccRCC by stimulating EMT and activating the Wnt/β-catenin pathway, ultimately enhancing tumor aggressiveness and metastatic potential. Thus, targeting ARPC1B represents a promising therapeutic strategy, warranting further exploration in ccRCC management.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"3127-3154"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233055","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":"Cancer 3D Models: Essential Tools for Understanding and Overcoming Drug Resistance.","authors":"Sofija Jovanović Stojanov, Marija Grozdanić, Mila Ljujić, Sandra Dragičević, Miodrag Dragoj, Jelena Dinić","doi":"10.32604/or.2025.067126","DOIUrl":"10.32604/or.2025.067126","url":null,"abstract":"<p><p>Anticancer drug resistance remains a major challenge in cancer treatment hindering the efficacy of chemotherapy and targeted therapies. Conventional two-dimensional (2D) cell cultures cannot replicate the complexity of the <i>in vivo</i> tumor microenvironment (TME), limiting their utility for drug resistance research. Therefore, three-dimensional (3D) tumor models have proven to be a promising alternative for investigating chemoresistance mechanisms. In this review, various cancer 3D models, including spheroids, organoids, scaffold-based models, and bioprinted models, are comprehensively evaluated with a focus on their application in drug resistance studies. We discuss the materials, properties, and advantages of each model, highlighting their ability to better mimic the TME and represent complex mechanisms of drug resistance such as epithelial-mesenchymal transition (EMT), drug efflux, and tumor-stroma interactions. Furthermore, we investigate the limitations of these models, including scalability, reproducibility and technical challenges, as well as their potential therapeutic impact on personalized medicine. Through a thorough comparison of model performance, we provide insights into the strengths and weaknesses of each approach and offer guidance for model selection based on specific research needs.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2741-2785"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233105","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 AMPK for Cancer Therapy: Metabolic Reprogramming as a Therapeutic Strategy.","authors":"Minseo Hong, Jea-Hyun Baek","doi":"10.32604/or.2025.067487","DOIUrl":"10.32604/or.2025.067487","url":null,"abstract":"<p><p>AMP-activated protein kinase (AMPK) is a highly conserved serine/threonine kinase that functions as a central regulator of cellular energy status. In cancer, where metabolic reprogramming enables rapid proliferation and survival under stress, AMPK functions as a metabolic checkpoint that restrains tumor growth by inhibiting biosynthetic pathways and promoting catabolic processes, such as autophagy and fatty acid oxidation. Given its role in opposing many hallmarks of cancer metabolism, AMPK has attracted significant interest as a therapeutic target. This review examines the molecular mechanisms by which AMPK influences tumor progression and evaluates the preclinical and clinical evidence for pharmacological AMPK activation using agents such as metformin, phenformin, and canagliflozin. While promising anti-tumor effects have been reported in specific contexts-such as HER2-positive breast cancer, colorectal cancer, and metabolically distinct lung cancer subtypes-clinical efficacy remains variable. Limitations include indirect activation mechanisms, low tissue penetrance, tumor heterogeneity, and lack of reliable biomarkers for patient selection. We discuss emerging strategies to overcome these challenges, including combination therapies, metabolic stratification, and the development of direct AMPK activators or mRNA-based delivery platforms. Together, these insights support a renewed focus on AMPK as a modifiable node in cancer metabolism and a candidate for integration into precision oncology frameworks.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 10","pages":"2699-2724"},"PeriodicalIF":4.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233176","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":"Inhibition of Proteasome LMP2 Activity Suppresses <i>Chil3</i> Expression in Mouse Colon Adenocarcinoma Tissue and Restrains Tumor Growth.","authors":"Tatiana M Astakhova, Nikita S Karpov, Nataliya O Dashenkova, Elena V Alpeeva, Mikhail V Nesterchuk, Sergey B Akopov, Arsen S Mikaelyan, Anfisa S Ryabchenko, Pavel A Erokhov, Natalia P Sharova","doi":"10.32604/or.2025.066611","DOIUrl":"10.32604/or.2025.066611","url":null,"abstract":"<p><strong>Objectives: </strong>Proteasomes, multi-subunit proteases, are key actors of cellular protein catabolism and a number of regulatory processes. The detection of subtle proteasome functioning in tumors may contribute to our understanding of the mechanisms of cancer development. The current study aimed to identify the role of low molecular mass protein 2 (LMP2), a proteasome immune subunit, in the development of mouse colon 26 (C26) adenocarcinoma.</p><p><strong>Methods: </strong>The functions of the LMP2 subunit in tumor development in Balb/c mice were studied using its irreversible inhibitor KZR-504. LMP2 activity was detected by the hydrolysis of the fluorogenic substrate Ac-Pro-Ala-Leu-AMC. Western blotting and Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR) were used. We applied fluorescent tests for cell proliferation and apoptosis. M2 macrophages were obtained by polarization of mouse bone marrow-derived macrophages using the corresponding cytokines.</p><p><strong>Results: </strong>KZR-504 showed high specificity only for the LMP2 subunit and had no negative effect on C26 cells in culture. However, KZR-504 suppressed the formation of tumor conglomerates (by 74%, <i>p</i> < 0.001) after C26 cell transplantation <i>in vivo</i>, inhibited the expression of chitinase-3-like protein 3 (Chil3) gene (by 90%, <i>p</i> < 0.001), a key marker of immunosuppressive M2 macrophages, in the tumor microenvironment, and reduced the tumor weight compared to the control (by 48%, <i>p</i> < 0.01). KZR-504 also suppressed the expression of <i>Chil3</i> (by 68%, <i>p</i> < 0.05) and arginase-1 (Arg1) (by 90%, <i>p</i> < 0.001), another marker gene, in M2 macrophages and violated M0-M2 macrophage polarization in culture.</p><p><strong>Conclusion: </strong>We discovered earlier unknown functions of the proteasome LMP2 subunit to facilitate the formation of tumor conglomerates and maintain <i>Chil3</i> and <i>Arg1</i> expression in immunosuppressive M2 macrophages. Our work demonstrates that the proteasome LMP2 subunit can be a target for antitumor treatment.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2573-2595"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015916","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":"TIMM8A-TIMM13 Complex Exerts Oncogenic Functions in Lung Cancer.","authors":"Shengmin Li, Kejian Shi, Ying Wang, Yi Zhang","doi":"10.32604/or.2025.063812","DOIUrl":"10.32604/or.2025.063812","url":null,"abstract":"<p><strong>Objectives: </strong>Lung cancer represents a major global healthcare challenge, characterized by high annual incidence and mortality rates worldwide. Although targeted therapies for lung cancer have advanced, treatment outcomes for advanced-stage patients remain suboptimal. This investigation examines the role of the translocase of the inner mitochondrial membrane (TIMM)8A-TIMM13 complex in lung cancer and evaluates its potential as a novel therapeutic target.</p><p><strong>Methods: </strong>A co-immunoprecipitation (Co-IP) assay was conducted to verify the interaction between TIMM8A and TIMM13. Differential gene expression analysis of TIMM8A or TIMM13 was executed using the TNMplot database, with survival estimates derived from the Kaplan-Meier plotter. Lung cancer cell proliferation was evaluated through Cell Counting Kit 8 (CCK-8) and colony formation assays, while cell migration was assessed via Transwell assay. RNA sequencing identified the downstream effectors of TIMM13. RNAi technology facilitated the inhibition of TIMM8A or TIMM13 expression, which was measured through immunoblotting or qRT-PCR.</p><p><strong>Results: </strong>This investigation revealed that components of the TIMM8A-TIMM13 complex exhibited elevated expression in human lung cancer tissues, correlating with disease progression and poor overall survival rates among lung cancer patients. The suppression of either TIMM8A or TIMM13 inhibited cell proliferation and migration. Mechanistic studies through transcriptome analysis identified cell cycle-related pathways as potential key downstream effectors of the TIMM8A-TIMM13 complex. Subsequent experiments confirmed that the TIMM8A-TIMM13 complex significantly regulated the expression of cyclin D1 (CCND1) and cyclin-dependent kinase 6 (CDK6) complex.</p><p><strong>Conclusion: </strong>The elevated expression of TIMM8A-TIMM13 complex components plays a crucial role in lung cancer cell growth, suggesting its potential as a promising therapeutic target for lung cancer treatment.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2435-2449"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015952","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":"Retraction: Long Noncoding RNA GAS5 Suppresses Tumorigenesis by Inhibiting miR-23a Expression in Non-Small Cell Lung Cancer.","authors":"","doi":"10.32604/or.2025.071884","DOIUrl":"https://doi.org/10.32604/or.2025.071884","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504016X14822800040451.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2599"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015929","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":"Polyphenols in Pancreatic Cancer Management: Exploring the Roles and Mechanisms of Resveratrol and Epigallocatechin.","authors":"David A de la Garza-Kalife, Verónica L Loaiza-Gutiérrez, Esther Alhelí Hernández-Tobías, Carlos A González-Villarreal, Jose Francisco Islas, Michelle G Santoyo-Suárez, Elsa N Garza-Treviño, Paulina Delgado-Gonzalez","doi":"10.32604/or.2025.065222","DOIUrl":"10.32604/or.2025.065222","url":null,"abstract":"<p><p>Emerging evidence highlights the potential of bioactive compounds, particularly polyphenols, as adjunctive therapeutic agents in the treatment of pancreatic cancer (PC), one of the most aggressive malignancies. This review focuses on epigallocatechin gallate (EGCG) and resveratrol due to their extensively documented anticancer activity, favorable safety profiles, and their unique ability to modulate multiple signaling pathways relevant to pancreatic tumorigenesis. Among polyphenols, these two have shown superior anti-cancer activity, epigenetic regulatory effects, and synergy with standard chemotherapies in preclinical pancreatic cancer models. Resveratrol exhibits anti-proliferative effects by modulating key signaling pathways, including phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt), nuclear factor kappa-B (NF-κB), and tumor protein 53 (p53). EGCG exerts anti-cancer activity by targeting multiple cellular processes, such as oxidative stress reduction, and suppression of inflammatory mediators like Interleukin-6 (IL-6) and Tumor Necrosis Factor-α (TNF-α). Both EGCG and resveratrol exert anti-pancreatic cancer effects partly through direct interactions with cell surface receptors and modulation of intracellular cascades. EGCG targets the 67 kDa laminin receptor (67LR), which is overexpressed in pancreatic cancer cells, triggering apoptosis, cyclic guanosine monophosphate (cGMP) production and activation of the PKCδ/acid sphingomyelinase (ASM) cascade. Resveratrol inhibits insulin-like growth factor-1 receptor (IGF-1R) activation of the PI3K/Akt and Wnt signaling pathways, while concurrently activating tumor suppressor p53. These interactions suppress proliferation, promote apoptosis, and reduce epithelial-mesenchymal transition (EMT), thereby limiting tumor progression. Both polyphenols enhance chemosensitivity and reduce resistance to conventional therapies, including gemcitabine, by modulating drug transporters and apoptotic pathways. Furthermore, their epigenetic influence, particularly via DNA methylation and histone modification, suggests a broader role in pancreatic cancer prevention. Understanding the roles and mechanisms of resveratrol and EGCG in pancreatic cancer provides valuable insights into novel treatment strategies. The integration of polyphenols into conventional therapeutic approaches may offer new hope for improving patient outcomes.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2243-2262"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015913","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":"Integrating Spatial Multi-Omics and Machine Learning to Unravel the Role of PANoptosis in Bladder Cancer Prognosis and Immunotherapy Response.","authors":"Liangju Peng, Tingting Cai, Peihang Xu, Cong Chen, Qingzhi Xiang, Yiping Zhu, Dingwei Ye, Yijun Shen","doi":"10.32604/or.2025.064331","DOIUrl":"10.32604/or.2025.064331","url":null,"abstract":"<p><p><b>Background:</b> Studies have reported the special value of PANoptosis in cancer, but there is no study on the prognostic and therapeutic effects of PANoptosis in bladder cancer (BLCA). This study aimed to explore the role of PANoptosis in BLCA heterogeneity and its impact on clinical outcomes and immunotherapy response while establishing a robust prognostic model based on PANoptosis-related features. <b>Methods:</b> Gene expression profiles and clinical data were collected from public databases. Spatial heterogeneity of cell death pathways in BLCA was evaluated. Consensus clustering was performed based on identified PANoptosis genes. Cell death pathway scores, molecular, and pathway activation differences between different groups were compared. Protein-protein interaction (PPI) network construction was constructed, and immune-related gene sets, tumor immune dysfunction and exclusion (TIDE) scores, and SubMap analysis were used to evaluate immunomodulator expression and immunotherapy efficacy. Ten machine learning algorithms were utilized to develop the most accurate predictive risk model, and a nomogram was created for clinical application. <b>Results:</b> BLCA demonstrated a spatially heterogeneous distribution of pyroptosis, apoptosis, and necroptosis. Notably, T effector cells significantly colocalized with total apoptosis. Two PANoptosis modes were identified: high PANoptosis (high. PANO) and low PANoptosis (low. PANO). High. PANO was associated with worse clinical outcomes and advanced tumor stage, and increased activation of immune-related and cell death pathways. It also showed increased infiltration of immune cells, elevated expression of immunomodulatory factors, and enhanced responsiveness to the immunotherapy. The PANoptosis-related machine learning prognostic signature (PMLS) exhibited strong predictive power for outcomes in BLCA. CSPG4 was identified as a key gene underlying prognostic and therapeutic differences. <b>Conclusion:</b> PANoptosis shapes distinct prognostic and immunological phenotypes in BLCA. PMLS offers a reliable prognostic tool. CSPG4 may represent a potential therapeutic target in PANoptosis-driven BLCA.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2463-2489"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015947","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":"Retraction: MicroRNA-221-3p Plays an Oncogenic Role in Gastric Carcinoma by Inhibiting PTEN Expression.","authors":"","doi":"10.32604/or.2025.071885","DOIUrl":"https://doi.org/10.32604/or.2025.071885","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504016X14756282819385.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2601"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016003","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}