Oncology reports最新文献

{"title":"BUB1B promotes homologous recombination‑mediated DNA damage repair in breast cancer cells through the PI3K/AKT signaling pathway.","authors":"Xuewen Luo, Yuqin Wei, Hanxin Lin, Ning Xiao, Wei Zhao","doi":"10.3892/or.2025.8980","DOIUrl":"10.3892/or.2025.8980","url":null,"abstract":"<p><p>Radioresistance is a major obstacle to effective radiotherapy in breast cancer. BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) is involved in numerous biological processes associated with cancer; however, its specific role in mediating radioresistance in breast cancer remains poorly characterized. The present study first evaluated its expression profile and association with patient prognosis through bioinformatics analysis. Subsequently, BUB1B expression in various breast cancer cell lines was validated by reverse transcription‑quantitative PCR. Following short hairpin RNA‑mediated knockdown of BUB1B in MDA‑MB‑231 cells, the impact of BUB1B on the biological functions and radiosensitivity of breast cancer cells was investigated using Cell Counting Kit‑8, colony formation, EdU staining, gap closure, Transwell, immunofluorescence and comet assays, flow cytometric cell cycle analysis, and <i>in vivo</i> xenograft tumor experiments. Downstream signaling pathways regulated by BUB1B were identified via RNA sequencing and western blotting. The results revealed that BUB1B expression was elevated in breast cancer tissues and cell lines, and higher BUB1B expression was associated with poorer prognosis in patients with breast cancer. Functional investigations demonstrated that BUB1B may facilitate the proliferation, invasion and migration of breast cancer cells. Furthermore, BUB1B had a significant influence on the radioresistance of breast cancer, and promoted homologous recombination‑mediated DNA damage repair and cell cycle arrest. At the molecular level, BUB1B may exert its effects through regulation of the PI3K/AKT signaling cascade. In conclusion, these findings indicated that BUB1B may be a potential therapeutic target to overcome radioresistance in breast cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145001006","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] Tumor‑released lncRNA H19 promotes gefitinib resistance via packaging into exosomes in non‑small cell lung cancer.","authors":"Yi Lei, Wang Guo, Bowang Chen, Lu Chen, Jiaxin Gong, Weimin Li","doi":"10.3892/or.2025.8973","DOIUrl":"10.3892/or.2025.8973","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 certain of the TEM microscopic data featured in Fig. 3C on p. 3443, the RIP assay data in Fig. 4A and the western blot data in Fig. 4D on p. 3444 were strikingly similar to data that had appeared in other articles written by different authors at different research institutes, which had either already been published before this article was received at <i>Oncology Reports</i>, or were submitted for publication at around the same time (one of which has subsequently been retracted).  Owing to the fact that certain of the abovementioned data had already been published prior to the receipt of this article at <i>Oncology Reports</i>, the Editor has decided that this paper should be retracted from the Journal. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 40: 3438‑3446, 2018; DOI: 10.3892/or.2018.6762].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144848189","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":"Emerging dual role of ferroptosis in lung cancer (Review).","authors":"Anqi Wu, Yingchen Ni, Youlang Zhou, Jiahai Shi","doi":"10.3892/or.2025.8974","DOIUrl":"10.3892/or.2025.8974","url":null,"abstract":"<p><p>Lung cancer (LC) is the second most frequently diagnosed malignancy worldwide and has the highest mortality rate among all types of cancer. Despite advancements in treatment strategies, the overall survival rate for affected individuals remains low. Ferroptosis, a form of regulated cell death characterized by iron‑dependent lipid peroxidation and accumulation of reactive oxygen species, serves a role in LC. The present review aimed to explore the dual role of ferroptosis in LC, examining both its pathological and therapeutic implications. Ferroptosis contributes to tumor progression, modulates the immune microenvironment and influences treatment resistance. Conversely, it also enhances the efficacy of immunotherapy, increases radiosensitivity and decreases chemotherapy resistance. The present study aimed to summarize the potential of ferroptosis‑based strategies, including the use of nanomaterials and combination therapy, to inform future research and therapeutic approaches.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12402756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963689","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":"Lactylation modification in lung cancer: A review of current research and future directions (Review).","authors":"Qingguo Lv, Jianan Xu, Na Hu, Yujun Zhao, Xin Wang, Tan Wang, Lin Tian","doi":"10.3892/or.2025.8981","DOIUrl":"10.3892/or.2025.8981","url":null,"abstract":"<p><p>Lung cancer is a common malignancy that poses risks to human health and quality of life. The primary treatment options currently available include surgery, chemotherapy and radiotherapy. However, the aggressive metastatic nature of the disease combined with the development of drug and radiation resistance results in suboptimal survival outcomes. Consequently, there is a need to explore novel therapeutic approaches and develop more effective drugs. Lactylation, an epigenetic modification induced by lactate, alters histone proteins to modify the chromatin structure, as well as non‑histone proteins. This post‑translational modification is associated with the initiation and progression of lung cancer. Lactylation carries out a considerable role in the onset, progression and resistance of the disease by influencing tumor metabolism and the surrounding microenvironment. Targeting lactylation could provide innovative strategies for the targeted therapy of lung cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145001020","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":"Ursolic acid: A natural pentacyclic triterpenoid with clinical promise in gynecological and breast cancers (Review).","authors":"Tingting Chen, Shirun Sun, Zhengli Zhou, Xiuqin Zhang","doi":"10.3892/or.2025.8986","DOIUrl":"10.3892/or.2025.8986","url":null,"abstract":"<p><p>Gynecological and breast cancers pose significant challenges to women's health worldwide. Despite notable advancements in diagnosis and treatment, they remain leading causes of cancer‑related mortality. Ursolic acid (UA), a naturally occurring pentacyclic triterpenoid widely found in plants, has garnered considerable attention due to its diverse pharmacological activities. It has been demonstrated that UA exhibits a range of biological effects, including antitumor, anti‑inflammatory, and antioxidant properties, with particularly promising therapeutic potential in breast and gynecological cancers. UA exerts its anticancer effects by modulating multiple signaling pathways, such as PI3K/AKT, NF‑κB, and Wnt/β‑catenin, thereby effectively inhibiting tumor cell proliferation, inducing apoptosis, reversing chemoresistance, and suppressing cancer stem cell characteristics. When combined with chemotherapeutic agents such as cisplatin and doxorubicin, UA not only enhances antitumor efficacy but also mitigates the adverse effects associated with chemotherapy. The present review summarizes the recent research progress and underlying mechanisms of UA in the treatment of gynecological and breast cancers, aiming to provide valuable insights for researchers and clinicians in the field.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12452220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040953","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":"DBN1‑mediated upregulation of GAB2 facilitates the migration and invasion of T‑cell acute lymphoblastic leukemia cells.","authors":"Jiaxing Sun, Xiaoxing Huang, Xingruo Zeng, Yufei Lei, Hengjing He, Zimeng Wei, Di Xiao, Qiuping Zhang, Xinran Li, Fuling Zhou, Liang Shao","doi":"10.3892/or.2025.8982","DOIUrl":"10.3892/or.2025.8982","url":null,"abstract":"<p><p>T-cell acute lymphoblastic leukemia (T‑ALL) is an aggressive hematological malignancy. The poor prognosis of T‑ALL is closely associated with extensive leukemic infiltration into critical organs. Therefore, the mechanism underlying T‑ALL infiltration is worth investigating. Databases and clinical samples were utilized to examine drebrin 1 (DBN1) expression in T‑ALL. DBN1 knockdown cell lines were established by lentivirus transfection, and cell migration and invasion were examined using Transwell and Matrigel‑Transwell assays. The molecular mechanism was investigated by RNA sequencing and further validated at the molecular level. Reverse transcription‑quantitative PCR and western blotting were employed to examine the expression of downstream molecules following DBN1 knockdown, with subsequent rescue experiments. DBN1‑targeting microRNA (miR) predicted using bioinformatics websites was confirmed using dual‑luciferase assays. In T‑ALL cells, miRNA mimics transfection enabled functional validation, and investigations into the underlying molecular mechanisms encompassing rescue experiments. Clinical samples and publicly available databases revealed that DBN1 was upregulated in patients with T‑ALL patients. DBN1 knockdown significantly decreased the migration and invasion of T‑ALL cells <i>in vitro</i>. RNA sequencing revealed that downregulation of DBN1 could reduce Grb2‑associated binding protein 2 (GAB2) expression. Western blotting revealed that GAB2 expression, and PI3K/AKT and MAPK/ERK signaling were decreased in DBN1‑knockdown cells. GAB2 overexpression restored the phosphorylation of downstream effectors (AKT and ERK1/2). Bioinformatics and dual‑luciferase reporter experiments identified miR‑218‑5p binding to the 3'-untranslated region of DBN1, which suppressed DBN1 expression. In addition, the experiments demonstrated that miR‑218‑5p acted as an upstream regulator of DBN1, and was involved in cell migration and invasion. Overall, DBN1 was upregulated in T‑ALL, and its depletion inhibited cell migration and invasion through downregulation of GAB2 and consequent inhibition of AKT and ERK signaling cascades. The present data suggested that DBN1 could be a novel biomarker of T‑ALL infiltration, which is a novel perspective in the field of leukemia research.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145001048","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] Src homology phosphotyrosyl phosphatase 2 mediates cisplatin‑related drug resistance by inhibiting apoptosis and activating the Ras/PI3K/Akt1/survivin pathway in lung cancer cells.","authors":"Chunlan Tang, Eunsil Hahm, Seyeon Bae, Jae Seung Kang, Wang Jae Lee","doi":"10.3892/or.2025.8979","DOIUrl":"10.3892/or.2025.8979","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 immunohistochemical images shown in Figs. 1E and 5E appeared to show an overlapping section, even though Figs. 1 and 5 were intended to show the results of SHP2 and Ras expression experiments, respectively. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, 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 continues to investigate this matter further. [Oncology Reports 39: 611‑618, 2018; DOI: 10.3892/or.2017.6109].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12412358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963694","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":"Circular RNAs in colorectal cancer: From molecular mechanisms to therapeutic applications (Review).","authors":"Yuxing He, Can Luo, Wei Du, Debei Liu, Lingshan Liao, Siqian Wang, Yanlin Cao","doi":"10.3892/or.2025.8972","DOIUrl":"10.3892/or.2025.8972","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) are stable, conserved non‑coding RNA molecules with key roles in gene regulation. Because of their tissue‑specific expression patterns and involvement in various cellular processes, circRNAs are relevant in cancer biology, specifically for colorectal cancer (CRC) diagnosis. The present review systematically examines the roles of circRNAs in CRC pathogenesis and their potential as diagnostic biomarkers and therapeutic targets for CRC, focusing on the key circRNAs involved in CRC development and progression, their molecular mechanisms and clinical value, as well as advances in circRNA‑based therapeutic strategies and challenges in the clinical translation of circRNA application.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144848190","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] Identification of TYMS as a promoting factor of retroperitoneal liposarcoma progression: Bioinformatics analysis and biological evidence.","authors":"Sha Zhang, Liang Yan, Can Cui, Zhen Wang, Jianhui Wu, Min Zhao, Bin Dong, Xiaoya Guan, Xiuyun Tian, Chunyi Hao","doi":"10.3892/or.2025.8968","DOIUrl":"10.3892/or.2025.8968","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, the authors contacted the Editorial Office to explain that, for the Transwell migration and invasion assay experiments shown in Fig. 4 on p. 573, the data panel for the '94T778 / Lenti‑shTYMS‑1' experiment shown in Fig. 4A was selected incorrectly. The authors have re‑examined their original data, and realize how this error occurred. The revised (and corrected) version of Fig. 4 shown on the next page. The authors sincerely apologize for the error introduced during the preparation of this figure, although they confirm that this did not grossly affect either the results or the conclusions reported in this study. They also thank the Editor of <i>Oncology Reports</i> for granting them the opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 44: 565‑576, 2020; DOI: 10.3892/or.2020.7635].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799689","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":"ISG20: The multifaceted 'molecular star' in cancer research (Review).","authors":"Xinhui Zhu, Shihao Jiang, Lipeng Zhang, Shaojian Zou, Houqin Zhang, Jingyu Zhang, Liyu Chen, Hui Li, Zhen Zong","doi":"10.3892/or.2025.8985","DOIUrl":"10.3892/or.2025.8985","url":null,"abstract":"<p><p>IFN‑stimulated gene (ISG)20 is a key member of the ISG family, serving a central role in antiviral defense, immune regulation and cell metabolism through its exonuclease activity. ISG20 is markedly dysregulated in various malignancies, including clear cell renal cell carcinoma, glioma, breast cancer and hepatocellular carcinoma, and it is associated with tumor proliferation, metastasis, angiogenesis and immune evasion. Its dual regulatory roles, such as promoting tumor progression via the MMP9/CCND1 signaling axis or enhancing antitumor immunity by activating the IFN‑β pathway, highlight its complex involvement in tumor biology. The present review aimed to summarize the discovery, structural characteristics and physiological functions of ISG20, and its multifaceted roles in tumor development. Moreover, the potential of ISG20 as a novel biomarker, immunoadjuvant and therapeutic target is discussed, offering theoretical insight and translational directions for precision oncology.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 5","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12452223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040866","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}