International journal of oncology最新文献

{"title":"Harnessing TP73‑targeted nintedanib: A novel strategy to halt triple‑negative breast cancer via p53‑PPARα/PI3K‑Akt pathway suppression.","authors":"Xiaomeng Zou, Shiyu Li, Sisi Huang, Ruilan Niu, Gang Liu, Zhili Wang","doi":"10.3892/ijo.2025.5794","DOIUrl":"10.3892/ijo.2025.5794","url":null,"abstract":"<p><p>Triple‑negative breast cancer (TNBC) is an aggressive malignancy with limited treatment options, leading to poor clinical outcomes and the need for novel therapeutic approaches. Nintedanib, a United States Food and Drug Administration‑approved multi‑kinase inhibitor with anti‑fibrotic and anti‑angiogenic properties, has shown promise in cancer treatment. However, its precise molecular effects on TNBC have not yet been fully elucidated. Therefore, the present study aimed to investigate the therapeutic potential of nintedanib in TNBC using <i>in vitro</i> and <i>in vivo</i> models, specifically focusing on its regulatory effects on key oncogenic pathways. The present study utilized TNBC cell lines (MDA‑MB‑231 and 4T1) and BALB/c mice to evaluate the antitumor efficacy of nintedanib. Cell viability and clonogenic capacity were assessed using Cell Counting Kit‑8 and colony formation assays. Subsequently, apoptosis induction and cell cycle progression were determined by flow cytometry, and cell migration and invasion were analyzed through scratch and Transwell assays. To identify underlying mechanisms, potential molecular targets were identified via bioinformatics and network pharmacology, and were validated through western blotting, immunofluorescence and immunohistochemistry. Finally, an orthotopic TNBC mouse model was established and monitored in real time by multimodal ultrasound imaging. The results revealed that nintedanib significantly inhibited TNBC cell proliferation and suppressed stem cell‑like properties. Furthermore, it induced cell cycle arrest at the G₂/M phase and promoted apoptosis. Mechanistic analysis revealed that nintedanib activated tumor protein p73 (TP73), leading to the disruption of the p53‑peroxisome proliferator‑activated receptor α (PPARα)/PI3K‑Akt signaling axis. Additionally, it downregulated epithelial‑mesenchymal transition (EMT) markers, including Snail and zinc finger E‑box‑binding homeobox protein 1, thereby mitigating tumor invasiveness. <i>In vivo</i>, nintedanib treatment effectively reduced tumor growth, angiogenesis and stiffness, indicating its potential as a viable therapeutic agent for TNBC. In conclusion, nintedanib exerts potent anti‑TNBC effects by modulating TP73, disrupting oncogenic signaling via the p53‑PPARα/PI3K‑Akt axis, and attenuating EMT‑associated transcription factors. These findings highlight its potential as a promising targeted therapy for TNBC, warranting further clinical exploration.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12425344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953910","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] Furin promotes epithelial‑mesenchymal transition in pancreatic cancer cells via Hippo‑YAP pathway.","authors":"Youli Zhang, Meng Zhou, Hong Wei, Hailang Zhou, Junbo He, Ying Lu, Dawei Wang, Baoding Chen, Jian Zeng, Wanxin Peng, Fengyi Du, Aihua Gong, Min Xu","doi":"10.3892/ijo.2025.5797","DOIUrl":"10.3892/ijo.2025.5797","url":null,"abstract":"<p><p>Following the publication of the above article, the authors drew to the Editor's attention that the image in Fig. 3A on p. 1356 for the 'Migration/BxPC3/sh‑EGFP' experiment was mistakenly presented. This error arose as a consequence of a mistake that was made during the preparation of the final images. Furthermore, upon performing an independent analysis of the data in this paper in the Editorial Office, it came to light that, for the colony‑formation assay experiments shown in Fig. 2F on p. 1355, the image selected for the 'PaTu8988/Flag‑Furin' experiment had already appeared in a different context in another paper published by the same authors, also in the journal <i>International Journal of Oncology</i>. After having examined their original data, the authors realize that this second figure in the paper had also been inadvertently assembled incorrectly. The revised versions of Fig. 2 (now showing the data correctly for the for the 'PaTu8988/Flag‑Furin' experiment) and Fig. 3 (showing the correct data for the 'Migration/BxPC3/sh‑EGFP' experiment) are shown on the next two pages. Note that the errors made during the compilation of these figures did not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of <i>International Journal of Oncology</i> for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 50: 1352‑1362, 2017; DOI: 10.3892/ijo.2017.3896].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953830","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":"Lp‑PLA2 in the cancer landscape: From molecular mechanisms to therapeutic potential (Review).","authors":"Xiaorong Yang, Yongbo Tu, Na Liang, Lingli Li, Jian Zhang, Jingyu Xu, Chunming Li","doi":"10.3892/ijo.2025.5793","DOIUrl":"10.3892/ijo.2025.5793","url":null,"abstract":"<p><p>Lipoprotein‑associated phospholipase A2 (Lp‑PLA2), an important member of the phospholipase A2 superfamily, was originally investigated for its proinflammatory role in cardiovascular diseases. Recent studies have revealed its significant role in tumorigenesis: It can act as either a tumor promoter or a tumor suppressor depending on the context. The present review systematically outlined the dual mechanisms by which Lp‑PLA2 contributes to cancer pathogenesis. As a tumor promoter, it promotes cancer progression via the induction of epithelial‑mesenchymal transition, glutathione peroxidase 4‑mediated resistance to ferroptosis, and vascular endothelial growth factor‑-dependent angiogenesis; conversely, as a tumor suppressor, it inhibits tumor growth by suppressing the Wnt/β‑catenin pathway in breast cancer gene 1‑mutated cancers or by promoting apoptosis. Mechanistic investigations clarify the interactions between Lp‑PLA2 and critical oncogenic pathways, such as the Notch and HIF1α pathways, while emphasizing the functional dichotomy that is influenced by the microenvironment. Current evidence supports the development of microenvironment‑guided targeting strategies and the potential value of Lp‑PLA2 as a prognostic biomarker and therapeutic target. These findings contribute to a theoretical framework for comprehending the context‑dependent roles of Lp‑PLA2 and may guide the development of innovative therapeutic approaches.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12425350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953924","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":"Cooperation between ZEB2 and SP1 upregulates PD‑L1 and CCL2 to promote the immunosuppressive activity of tumor cells.","authors":"Dongjoon Ko, Yunhee Lee, Junghwa Yoon, Eun Kyoung Choi, Donghwan Jang, Semi Kim","doi":"10.3892/ijo.2025.5801","DOIUrl":"10.3892/ijo.2025.5801","url":null,"abstract":"<p><p>Epithelial‑mesenchymal transition (EMT) is implicated in tumor progression and EMT‑inducing transcription factors play multifaceted roles; however, the molecular mechanisms underlying these processes are not well understood. Previously, we showed that ZEB2 acts cooperatively with the transcription factor SP1 to function as a transcriptional activator that promotes cancer cell invasion and survival, as well as angiogenesis. The present study reported a novel role for Zinc Finger E‑Box Binding Homeobox 2 (ZEB2) in conferring immunosuppressive activity on cancer cells, as well as the underlying molecular mechanism. ZEB2 cooperated with SP1 to upregulate transcription of <i>CD274</i> and <i>CCL2</i> by interacting with the proximal SP1 element in their promoters. ZEB2‑mediated programmed cell death 1 ligand 1 (PD‑L1) upregulation on tumor cells inhibited T cell activation and cytokine secretion in a co‑culture system. ZEB2 upregulated C‑C motif chemokine ligand 2 (CCL2) secretion to promote migration of macrophages and drive polarization to an M2‑like phenotype. ZEB2 suppressed the activity of tumor‑infiltrating T cells in a syngeneic mouse tumor model. Furthermore, SUMOylation of ZEB2 by PC2 was required for efficient cooperation between ZEB2 and SP1, as well as for subsequent gene expression. Clinical data showed that <i>ZEB2</i> expression is associated positively with expression of <i>CD274</i> and <i>CCL2</i>. Expression of both <i>ZEB2</i> and <i>CD274</i> or <i>CBX4</i> has prognostic significance for predicting survival of colon cancer patients. The present study demonstrated a previously unrecognized role for ZEB2: Direct modulation of the interaction between tumor cells and immune cells. Taken together, the data increased our understanding of the molecular mechanism underlying immunosuppression mediated by an EMT‑inducing transcription factor.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086218","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] Lithium chloride induces mesenchymal‑to‑epithelial reverting transition in primary colon cancer cell cultures.","authors":"Valeria Costabile, Francesca Duraturo, Paolo Delrio, Daniela Rega, Ugo Pace, Raffaella Liccardo, Giovanni Battista Rossi, Rita Genesio, Lucio Nitsch, Paola Izzo, Marina De Rosa","doi":"10.3892/ijo.2025.5800","DOIUrl":"10.3892/ijo.2025.5800","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew the authors' attention to the fact that the CTK18 panel in Fig. 2E on p. 1917, showing the results of RT‑PCR analysis of cytokeratin 18 from patient no. 88, appeared to be very similar to the CTK18 panel in Fig. 2F (showing the results from patient no. 93). After having re‑examined their original data, which were also presented to the Editorial Office, and considering that the observed experiment is an end-point RT-PCR performed more than ten years ago, the authors cannot definitively rule out the possibility that Fig. 2E was inadvertently misassembled. Therefore, given the high similarity of the two images, it was decided to publish a revised version of Fig. 2, which now shows data from a different replicate of the experiment for the CTK18 panel in Fig. 2E, shown on the next page. Note that this revision did not affect the overall conclusions reported in the study. The authors are grateful to the Editor of <i>International Journal of Oncology</i> for allowing them this opportunity to publish a Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 46: 1913‑1923, 2015; DOI: 10.3892/ijo.2015.2911].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040047","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":"[Expression of Concern] MicroRNA‑195 targets VEGFR2 and has a tumor suppressive role in ACHN cells via PI3K/Akt and Raf/MEK/ERK signaling pathways.","authors":"Pengcheng Sun, Lu Wang, Yunhan Lu, Yuwei Liu, Lechen Li, Luyao Yin, Cheng Zhang, Weiming Zhao, Baozhong Shen, Wanhai Xu","doi":"10.3892/ijo.2025.5792","DOIUrl":"10.3892/ijo.2025.5792","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the Transwell migration and invasion assay data shown in Fig. 3A and B, two pairs of panels appeared to contain overlapping sections of data (out of a total of ten panels), such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original sources. Upon analyzing the data independently in the Editorial Office, a third pair of data panels in the same figure were found to be similarly affected. The authors were contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Oncology 49: 1155‑1163, 2016; DOI: 10.3892/ijo.2016.3608].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12425347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953901","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":"[Expression of Concern] 4‑Hydroxybutenolide impairs cell migration, and invasion of human oral cancer SCC‑4 cells via the inhibition of NF‑κB and MAPK signaling pathways.","authors":"Fu-Shun Yu, Meng-Liang Lin, Shu-Chun Hsu, Chien-Chih Yu, Yi-Ping Huang, Yueh-Hsiung Kuo, Jing-Gung Chung","doi":"10.3892/ijo.2025.5795","DOIUrl":"10.3892/ijo.2025.5795","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell assay data shown in Fig. 2C on p. 582, the '24 h/1 <i>µ</i>M' and '24 h/2.5 <i>µ</i>M' data panels contained an overlapping section of cellular data; in addition, the '24 h/Control' and '48 h/Control' panels in Fig. 2E similarly contained an overlapping section of data, such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original sources. Upon analyzing the data independently in the Editorial Office, it came to light that the '0 h/1 <i>µ</i>M' and '12 h/2.5 <i>µ</i>M' data panels in Fig. 2A (showing the results of scratch‑wound assay experiments) also contained an overlapping area, albeit the 12 h/2.5 <i>µ</i>M' data panel had been rotated through 180° relative to the '0 h/1 <i>µ</i>M' panel.  The authors were contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Oncology 49: 579‑588, 2016; DOI: 10.3892/ijo.2016.3537].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12425337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953916","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":"Notch3 mediated TGF‑β1 activation enhances epithelial‑mesenchymal transition and cancer stemness in non‑small lung cancer.","authors":"Fang Wang, Siqi Hu, Jiangrong Bian, Qing Gao, Liuzhao Cao, Linli Sang, Junjun Yang, Xingxiang Xu","doi":"10.3892/ijo.2025.5791","DOIUrl":"https://doi.org/10.3892/ijo.2025.5791","url":null,"abstract":"<p><p>Notch3 is a key regulator in various cancers, playing a crucial role in maintaining stemness and promoting epithelial‑mesenchymal transition (EMT). However, its differential expression and regulatory mechanisms in non‑small cell lung cancer (NSCLC) and cancer stem cells remain poorly understood. To investigate this, the present study examined Notch3 expression in NSCLC through Oncomine, The Cancer Genome Atlas and Gene Expression Omnibus databases and validated the results with immunohistochemistry, reverse transcription‑quantitative PCR and western blotting. EMT was induced by TGF‑β1 in NSCLC cells and functional assays (Transwell, wound healing and sphere formation) were performed to assess cellular changes. <i>In vivo</i> experiments using a xenograft mouse model were conducted to evaluate tumor growth and metastasis. The results showed that high Notch3 expression was associated with poor prognosis in NSCLC patients. Downregulation of Notch3 inhibited TGF‑β1‑induced EMT and CSC characteristics, resulting in reduced tumorigenic potential, whereas overexpression of the Notch3 intracellular domain enhanced these effects. Silencing Notch3 suppressed EMT and markedly inhibited tumor growth and metastasis <i>in vivo</i>. These findings demonstrated that Notch3 regulated EMT and CSC properties in NSCLC, promoting tumor recurrence and metastasis. Notch3 thus represents a promising therapeutic target and prognostic marker for NSCLC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 4","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12370359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953819","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":"[Expression of Concern]  ETS‑1: A potential target of glycolysis for metabolic therapy by regulating glucose metabolism in pancreatic cancer.","authors":"Xiu Zhang, Dan Wu, Mohanad Aldarouish, Xiaodong Yin, Chunyan Li, Cailian Wang","doi":"10.3892/ijo.2025.5786","DOIUrl":"10.3892/ijo.2025.5786","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the western blots shown in Figs. 4B and 5B, the AMPK panel in Fig. 4B looked strikingly similar to the ATG5 panel in Fig. 5B, and the p‑AMPK panel in Fig. 4B looked highly similar to the ATG7 panel in Fig. 5B. The authors were contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Oncology 50: 232-240, 2017; DOI: 10.3892/ijo.2016.3770].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 4","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12370366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144846560","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":"Functional mechanisms of circular RNA‑encoded peptides and future research strategies and directions in nasopharyngeal carcinoma (Review).","authors":"Weihua Xu, Zhichao Ma, Wei Gong, Shengmiao Fu, Xinping Chen","doi":"10.3892/ijo.2025.5788","DOIUrl":"https://doi.org/10.3892/ijo.2025.5788","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC) is an epithelial malignancy closely associated with Epstein‑Barr virus (EBV) infection. Although patients with early‑stage NPC can achieve a high cure rate through radiotherapy, recurrence and distant metastasis remain the primary causes of treatment failure in patients with advanced‑stage NPC. Circular RNA (circRNA) is a class of covalently closed non‑coding RNAs involved in multiple aspects of tumor biology. Recent evidence has shown that certain circRNAs can encode functional peptides, which participate in the regulation of tumor‑related signaling pathways. In NPC, circRNAs have been implicated in the modulation of signaling pathways, including NF‑κB and JAK/STAT, both of which are activated in the EBV‑infected microenvironment. Furthermore, frequently mutated genes in NPC, such as TNF receptor‑associated factor 3 and cylindromatosis lysine 63 deubiquitinase, are known regulators of the NF‑κB pathway, suggesting a potential link between genetic alterations and circRNA‑related mechanisms. This article systematically reviews the biological mechanisms of circRNA‑encoded peptides, summarizes the expression and function of circRNA in NPC and focuses on discussing the potential roles of circRNA‑encoded peptides in tumor microenvironment regulation, immune escape and clinical application prospects. By integrating existing research results, this article aims to provide a new perspective and theoretical basis for the in‑depth exploration of circRNA‑encoded peptides in the field of NPC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 4","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12370367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953867","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}