Oncology reports最新文献

{"title":"[Corrigendum] 2'‑Hydroxyflavanone inhibits epithelial‑mesenchymal transition, and cell migration and invasion via suppression of the Wnt/β‑catenin signaling pathway in prostate cancer.","authors":"Shiqi Wu, Jun Huang, Ke Hui, Yangyang Yue, Yanan Gu, Zhongyun Ning, Xinyang Wang, Dalin He, Kaijie Wu","doi":"10.3892/or.2025.8935","DOIUrl":"10.3892/or.2025.8935","url":null,"abstract":"<p><p>Following the publication of the above article, the authors contacted the Editorial Office to explain that they had made inadvertent errors in compiling the scratch‑wound assay images in Fig. 1B on p. 2838 and Fig. 4A on p. 2840; essentially, the same data had been included for the '2HF, 10 µM, 0 h' and '2HF, 5 µM, 12 h' experiments in Fig. 1B, and for the 'Vector, 2HF, 5 µM, 12 h' and '2HF, 5 µM, 24 h' experiments in Fig. 4A. However, the authors were able to re‑examine their original data, and realized how these errors had occurred. The revised and corrected versions of Figs. 1 and 4, now including replacement data for the experiments with the PC‑3 cell line (lower panel) in Fig. 1B and the Vector experiments with the DU145 cell line in Fig. 4A, are shown on the next two pages. Note that the errors made with the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors apologize to the Editor of <i>Oncology Reports</i> and to the readership for any inconvenience caused. [Oncology Reports 40: 2836‑2843, 2018; DOI: 10.3892/or.2018.6678].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507316","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":"SENP1: A perspective from immune cells to disease (Review).","authors":"Xiaofang Feng, Guoyu Wu, Qiyan Zeng","doi":"10.3892/or.2025.8947","DOIUrl":"10.3892/or.2025.8947","url":null,"abstract":"<p><p>Small ubiquitin‑like modifier (SUMO) is a ubiquitin‑like protein that modifies target proteins across various eukaryotic subcellular structures. This process, known as SUMOylation, has been established as an essential regulatory mechanism that affects both the activity and positioning of proteins, maintaining cellular homeostasis. SUMOylation and deSUMOylation are reversible post‑translational modification processes mediated by SUMO proteins and SUMO/sentrin‑specific proteases (SENPs). The human SENP family comprises six members, each characterized by unique cellular localization and substrate specificity. The present review primarily summarizes the role and mechanisms of SENP1 in the development and maturation of immune cells, including lymphocytes, macrophages and erythrocytes, as well as its involvement in tumor cell invasion, metastasis, angiogenesis and resistance to pharmacological therapies. In addition, the introduction of SENP1 inhibitors as a therapeutic approach for cancer treatment is explored. Overall, the present study aimed to offer theoretical insights into cancer therapy strategies that target SENP1.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12288635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668041","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":"Comprehensive <i>in‑silico</i> molecular analysis of early‑onset gastric cancer identifies novel genes implicated in disease characterization and progression (Review).","authors":"Fernán Gómez-Valenzuela, Ian Silva, Ignacio N Retamal, Benjamín García-Bloj, Tomás De Mayo Glasser, Matías Muñoz-Medel, Alex Gómez, Cristopher San Martín, Carolina Sánchez, Felipe Pinto, Paola Aravena, Andrea C Sabioncello, Marcelo Garrido Villanueva, Fernando Sigler Chávez, Ignacio Corvalán, Henry Barrios, José M Erpel, Patricio A Manque, Juan A Godoy, Marcelo Garrido","doi":"10.3892/or.2025.8931","DOIUrl":"10.3892/or.2025.8931","url":null,"abstract":"<p><p>Gastric cancer, a prevalent and fatal form of cancer worldwide, is manifested at different age ranges during the lifespan. Approximately one‑third of newly diagnosed gastric cancer cases are early‑onset gastric cancer (EO‑GC), which affects individuals under the age of 50 years. EO‑GC tends to be more aggressive than late‑onset gastric cancer (L‑GC), with a faster and multifocal disease progression. Furthermore, EO‑GC is associated with early metastatic disease. Recent research has underscored the need for a deeper understanding of EO‑GC that promotes therapeutic approaches specific to EO‑GC. The present study determined the main transcriptomic differences between EO‑GC and L‑GC. Transcriptomic expression data from The Cancer Genome Atlas‑Stomach Adenocarcinoma were explored to elucidate whether age is associated with a specific genomic expression pattern and is associated with gastric cancer. Subsequently, a differential gene expression analysis of the EO‑GC vs. L‑GC groups was performed, providing new insights into EO‑GC gene expression characteristics and their association with survival outcomes. Furthermore, the study focused on whether the influence of representative gene expression in EO‑GC cases (<i>KLHL4, MAGEL2, CYP8B1, RNLS, CLDN6, MIOX, PNMA5</i> and <i>ACTL8</i> genes) may be associated with its aggressive phenotype and methylation profiles of these patients. In this review, the necessity of incorporating age as a crucial element in understanding the disparities in outcomes for EO‑GC cases in public datasets was discussed. Furthermore, this insight may be useful for targeted early personalized clinical interventions to improve patient prognosis and survival rates in EO‑GC cases.</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/PMC12199296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333635","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] Cinobufagin induces autophagy‑mediated cell death in human osteosarcoma U2OS cells through the ROS/JNK/p38 signaling pathway.","authors":"Kun Ma, Chuan Zhang, Man-Yu Huang, Wu-Yin Li, Guo-Qiang Hu","doi":"10.3892/or.2025.8928","DOIUrl":"10.3892/or.2025.8928","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 cellular data shown in Fig. 2C on p. 93 had already been submitted to another journal in an article written by different authors at different research institutes, which has subsequently been retracted. Moreover, upon performing an independent assessment of the data in the above paper in the Editorial Office, it emerged that flow cytometric data in Figs. 1 and 4 were also strikingly similar to data appearing in other unrelated articles, and western blot data appeared to have been shared between Fig. 6A and E on p. 97, where the results from differently performed experiments were intended to have been portrayed. Owing to the fact that the contentious data in the above article had already been submitted to/published in unrelated articles, and given the fact that Fig. 6 had clearly been assembled incorrectly, the Editor of <i>Oncology Reports</i> has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 36: 90‑98, 2016; DOI: 10.3892/or.2016.4782].</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/PMC12183500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333583","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":"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":"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":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12174970/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"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":"<i>In vitro</i> assessment of BBI608 in 2D and 3D culture models for drug repositioning in oral squamous cell carcinoma.","authors":"Dong-Guk Park, Hyun-Ji Kim, Sak Lee, Hye-Mi Jiang, Seong-Doo Hong, Su-Jung Choi, Sung-Dae Cho","doi":"10.3892/or.2025.8930","DOIUrl":"10.3892/or.2025.8930","url":null,"abstract":"<p><p>STAT3 is abnormally activated in several types of cancer, and elevated nuclear levels of STAT3 are strongly associated with poor prognosis in oral squamous cell carcinoma (OSCC). Despite ongoing progress in developing targeted therapies, there is no Food and Drug Administration‑approved drug currently targeting STAT3 in OSCC. To evaluate the anticancer effects of BBI608, a potent STAT3 inhibitor, in two human OSCC cell lines (HSC‑3 and HSC‑4), various two‑dimensional (2D) or 3D <i>in vitro</i> analyses were performed, including western blot analysis, colony formation assay, DAPI staining, sub‑G₁ population analysis and Annexin V/PI staining. The molecular mechanisms of BBI608 were also determined using cross‑linking assay, nuclear and cytoplasmic fractionation assay, reverse transcription‑quantitative PCR and chromatin immunoprecipitation assay. In the present study, it was observed that human HSC‑3 and HSC‑4 OSCC cells exhibited higher levels of phosphorylated (p)‑STAT3 compared with those in immortalized oral keratinocytes (iHOK cells). BBI608 inhibited cell proliferation in a concentration‑dependent manner and triggered caspase 3‑dependent apoptosis in HSC‑3 and HSC‑4 cells. Additionally, BBI608 reduced the nuclear translocation of p‑STAT3 in HSC‑3 and HSC‑4 cells compared with that in DMSO‑treated cells. Mechanistically, BBI608 modulated anti‑apoptotic STAT3 downstream genes: Survivin expression was regulated at the transcriptional level, while myeloid cell leukemia‑1 expression was modulated post‑translation via proteasomal degradation. Consistent with the results from 2D culture, BBI608 showed effective anticancer effects against OSCC spheroids in 3D culture. These results suggest that BBI608 effectively inhibits STAT3 activation in both 2D and 3D models, offering a promising therapeutic strategy and supporting its potential for repurposing in patients with OSCC who exhibit elevated STAT3 activity.</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/PMC12203464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333634","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":"[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":"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":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175487/pdf/","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":"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}