{"title":"Prospects and applications of NK therapy in the treatment of gliomas (Review).","authors":"Yueyang Liu, Chen Su, Xiyao Wei, Ningbo Wei, Qijun Qian, Zenghui Xu","doi":"10.3892/or.2025.8921","DOIUrl":"10.3892/or.2025.8921","url":null,"abstract":"<p><p>Brain tumours are in the spotlight of oncology research due to their intractability and resistance to conventional treatments. High‑risk craniotomies must be performed on patients during tumour resection surgeries due to the specificity of the brain structure, and the complexity of the brain structure also leads to the fact that brain tumours usually cannot be removed completely. Besides, the inability of foreign small molecules to cross the blood‑brain barrier has led to the inability of conventional drug therapy to reach the tumour location in the brain. Furthermore, the damage to healthy brain tissue caused by conventional radiotherapy cannot be ignored. Therefore, brain tumours represented by gliomas are in urgent need for a novel therapeutic approach. Glioma is the most common brain tumour, accounting for 81% of malignant tumours in the central nervous system, and is characterized by high morbidity, recurrence, mortality and low cure rate. In recent years, natural killer (NK) cell immunotherapy for gliomas has gradually emerged and numerous studies have shown surprising therapeutic effects. NK cells have been demonstrated to traverse the blood‑brain barrier and numerous studies have confirmed their ability to kill glioma cells both <i>in vivo</i> and <i>in vitro</i>. This article begins by introducing conventional therapies for glioma, followed by an overview of the potential of NK cell‑based immunotherapy in glioma treatment and the regulatory mechanisms of NK cells within the glioma immune microenvironment. It then summarizes preclinical studies on CAR‑NK cells and clinical advancements in NK cell therapy for glioma. Finally, the paper discusses recent progress in immunotherapy for gliomas and explores novel therapeutic strategies combining NK cell immunotherapy with other treatment modalities.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12159591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Retracted] Formyl peptide receptor 2 expression predicts poor prognosis and promotes invasion and metastasis in epithelial ovarian cancer.","authors":"Xiaohui Xie, Mengyuan Yang, Yiling Ding, Ling Yu, Jianlin Chen","doi":"10.3892/or.2025.8922","DOIUrl":"https://doi.org/10.3892/or.2025.8922","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the authors had apparently compiled the Transwell assay data shown in Fig. 5C on p. 3304 incorrectly. Subsequently, the Editorial Office performed an independent analysis of the data shown in this paper, and this investigation revealed that certain of the tube formation assay data shown in Fig. 6 had apparently appeared in an article published in the journal <i>Molecular Medicine Reports</i> a few years previously, which had been written by different authors at different institutes. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Oncology Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 38: 3297‑3308, 2017; DOI: 10.3892/or.2017.6034].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oncology reportsPub Date : 2025-08-01Epub Date: 2025-05-30DOI: 10.3892/or.2025.8920
K M A Zinnah, Sang-Youel Park
{"title":"[Corrigendum] Sensitizing TRAIL‑resistant A549 lung cancer cells and enhancing TRAIL‑induced apoptosis with the antidepressant amitriptyline.","authors":"K M A Zinnah, Sang-Youel Park","doi":"10.3892/or.2025.8920","DOIUrl":"10.3892/or.2025.8920","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, for the cellular morphological images shown in Figs. 3A and 4A on p. 7 and 8 respectively, the centrally placed images (third from the left) were strikingly similar, such that the same data had apparently been included in these figures to show the results from differently performed experiments. After having re‑examined their original data files, the authors realized that the data panel in Fig. 4A properly belonged to Fig. 3, and that this image had been inadvertently included incorrectly in this figure. The revised version of Fig. 4, now featuring the correct data for the 'Amit+/TRAIL+/DR5 siRNA‑/NC ‑' experiment (third panel from the left), is shown on the next page. Note that the correction of this figure does not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 46: 144, 2021; DOI: 10.3892/or.2021.8095].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12150835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Involvement of the PRDX family and its clinical functions in different types of gastrointestinal cancer (Review).","authors":"Zhou Zhang, Yujie Wang, Yuhao Liu, Haizhen Wu, Xiaopeng Xu, Kai Wang, Chen He, Chen Qian","doi":"10.3892/or.2025.8923","DOIUrl":"10.3892/or.2025.8923","url":null,"abstract":"<p><p>Peroxiredoxin (PRDX) is a large and highly conserved family of peroxidases, which can maintain the dynamic balance of intracellular oxidative stress levels based on the degradation of the hydrogen peroxide, peroxynitrite and lipid peroxides, among others. Additionally, PRDXs are expressed with varying levels in almost all tumor tissues and cells, and they can regulate the downstream signaling cascades by modulating intracellular peroxide levels in tumor cells, alongside the participation during the modulation of gene expression, cell proliferation, apoptosis, migration, differentiation and other cellular biological behaviors. It has been revealed that the PRDXs family exhibits crucial functions in the occurrence, development, diagnosis and prognosis of gastrointestinal cancer, but a systematic summary was lacking in relevant studies. Therefore, the present study aims at probing into the underlying mechanisms of the PRDXs family in the occurrence and development of gastrointestinal cancer, providing new insights into the clinical diagnosis, treatment and prognosis monitoring.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Corrigendum] Arctigenin inhibits triple-negative breast cancers by targeting CIP2A to reactivate protein phosphatase 2A.","authors":"Qiuyue Huang, Shanshan Qin, Xiaoning Yuan, Liang Zhang, Juanli Ji, Xuewen Liu, Wenjing Ma, Yunfei Zhang, Pengfei Liu, Zhiting Sun, Jingxuan Zhang, Ying Liu","doi":"10.3892/or.2025.8925","DOIUrl":"https://doi.org/10.3892/or.2025.8925","url":null,"abstract":"<p><p>Following the publication of the above article, the authors drew to the Editor's attention that they has misclassified some of their original data, and this led to the erroneous compilation of the cell invasion and scratch wound assay data shown in Fig. 5A and B respectively on p. 604. Moreover, the authors realized that the same GAPDH control western blotting data had inadvertently been included in Fig. 4A and G on p. 603, where these data were correctly shown only for Fig. 4G. However, the authors had retained their original data for these figures, and the revised versions of Figs. 4 and 5, now showing the correct data for the GAPDH bands in Fig. 4A and the correct data for Fig. 5A and B, are shown on the next two pages. Note that the errors made in terms of the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of <i>Oncology Reports</i> for granting them this opportunity to publish a Corrigendum, and apologize to both the Editor and the readership for any inconvenience caused. [Oncology Reports 38: 598-606, 2017; DOI: 10.3892/or.2017.5667].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oncology reportsPub Date : 2025-08-01Epub Date: 2025-06-06DOI: 10.3892/or.2025.8924
Jiaqi Liu, Gejile Hu, Hua Du, Yingxu Shi
{"title":"Role and potential mechanisms of miR‑100 in different diseases (Review).","authors":"Jiaqi Liu, Gejile Hu, Hua Du, Yingxu Shi","doi":"10.3892/or.2025.8924","DOIUrl":"10.3892/or.2025.8924","url":null,"abstract":"<p><p>In recent years, the role of microRNAs (miRNAs) in disease has attracted considerable interest, underscoring their potential utility as diagnostic biomarkers. miR‑100, belonging to the miR‑99 family, is integral to the pathophysiological processes underlying numerous diseases. miR‑100 has been found to influence the pathogenesis of a variety of noncancerous diseases. As for cancer, this factor plays a significant role in various tumors throughout diverse systems, influencing essential processes including cell proliferation, invasion, migration and apoptosis of cancerous cells. This review examines the existing literature on miR‑100 in the context of non‑cancerous diseases and cancer, investigates its mechanisms of action across different diseases and considers its potential role as a diagnostic biomarker as well as its involvement in cancer drug resistance.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Crosstalk between cancer‑associated fibroblasts and inflammation in tumor microenvironment: A novel perspective in cancer therapy (Review).","authors":"Xinyan Liu, Chaofeng Wang, Huijuan Mao, Jianzi Wei","doi":"10.3892/or.2025.8926","DOIUrl":"https://doi.org/10.3892/or.2025.8926","url":null,"abstract":"<p><p>Inflammation is a hallmark of cancer, significantly contributing to tumor progression and therapeutic outcomes. Among the diverse cellular components of the tumor microenvironment, fibroblasts have been recognized as key regulators of inflammatory processes. Under tumor‑specific conditions, cancer‑associated fibroblasts (CAFs) undergo differentiation and promote tumor proliferation, metastasis and immune evasion <i>via</i> highly intricate mechanisms. This review provides a comprehensive analysis of the reciprocal interactions between CAFs and inflammation, elucidating the mechanisms by which CAFs induce pro‑inflammatory signaling and how inflammatory mediators, in turn, potentiate CAF activation and function. Furthermore, innovative therapeutic strategies, including the inhibition of stromal proteins, hypoxia‑inducible factor 1α and metabolic pathways associated with CAFs, as well as the application of nanoparticle‑based drug delivery systems, are examined for their potential to impede CAF‑mediated tumor progression. Pharmacological agents targeting CAF‑associated signaling pathways or inflammatory cytokines show dual efficacy by concurrently modulating inflammatory responses and CAF activity. These approaches frequently demonstrate improved therapeutic efficacy compared to interventions solely directed at CAF surface proteins, highlighting the therapeutic potential of concurrently addressing both inflammation and CAFs to enhance cancer treatment efficacy.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Corrigendum] Goserelin promotes the apoptosis of epithelial ovarian cancer cells by upregulating forkhead box O1 through the PI3K/AKT signaling pathway.","authors":"Ning Zhang, Junjun Qiu, Tingting Zheng, Xiaodan Zhang, Keqin Hua, Ying Zhang","doi":"10.3892/or.2025.8910","DOIUrl":"10.3892/or.2025.8910","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the authors' attention the fact that six consecutive β‑actin bands looked similar, comparing across panels in Fig. 6A and B on p. 1040, even though different time points were represented in these experiments. After having re‑examined their original data files, the authors realized that the β‑actin bands shown in Fig. 6A were inadvertently assembled incorrectly. The revised version of Fig. 6, now featuring the correct β‑actin blots for Fig. 6A, is shown on the next page. Note that the corrections made to this figure do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this further Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 39: 1034‑1042, 2018; DOI: 10.3892/or.2017.6159].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12079634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tryptophan metabolism: From physiological functions to key roles and therapeutic targets in cancer (Review).","authors":"Jiawei Zhao, Xiaohui Bai, Jingjing Du, Yujing Chen, Xiaotong Guo, Juzheng Zhang, Jinfeng Gan, Peitao Wu, Siqi Chen, Xinwen Zhang, Jinfeng Yang, Jiamin Jin, Li Gao","doi":"10.3892/or.2025.8919","DOIUrl":"10.3892/or.2025.8919","url":null,"abstract":"<p><p>Tryptophan (Trp) metabolism is a complex and important biochemical process in humans. It is vital in protein synthesis and is a precursor of various bioactive molecules. Trp is metabolized through the kynurenine, serotonin and indole pathways, mediating diverse physiological functions, including neurotransmitter synthesis, immune regulation, antioxidant effects, and biosynthesis of niacin and melatonin. These metabolic pathways maintain essential functions under normal physiological conditions. However, they are significantly affected by various types of cancers. Trp metabolites regulate tumor angiogenesis, affect the self‑renewal of cancer stem cells, and participate in immune evasion and cell death through complex mechanisms. As the mechanisms underlying Trp metabolism in diseases are increasingly being elucidated, targeting Trp metabolic pathways has emerged as a promising therapeutic strategy. Further investigation of the molecular mechanisms underlying Trp metabolism and its role in diseases may provide new perspectives and approaches for diagnosing and treating diseases.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oncology reportsPub Date : 2025-07-01Epub Date: 2025-05-16DOI: 10.3892/or.2025.8913
Hui Zhang, Hui Liu, Huaqiang Bi
{"title":"[Retracted] MicroRNA‑345 inhibits hepatocellular carcinoma metastasis by inhibiting YAP1.","authors":"Hui Zhang, Hui Liu, Huaqiang Bi","doi":"10.3892/or.2025.8913","DOIUrl":"10.3892/or.2025.8913","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the scratch wound assay data panels shown in Fig. 8B on p. 848 were strikingly similar to data which had appeared several years previously in Fig. 2A in another article written by different authors at different research institutes published in the journal <i>Therapeutics, Targets</i>, and <i>Chemical Biology.</i> In view of the fact that these data had already appeared in another publication prior to its submission to <i>Oncology Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 38: 843‑849, 2017; 10.3892/or.2017.5772].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12093927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}