Oncology reports最新文献

{"title":"[Expression of Concern] Hypoxia and macrophages promote glioblastoma invasion by the CCL4‑CCR5 axis.","authors":"Ying Wang, Tao Liu, Ning Yang, Shuo Xu, Xingang Li, Donghai Wang","doi":"10.3892/or.2025.8989","DOIUrl":"10.3892/or.2025.8989","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 'Normoxia / U87' panel in Fig. 1A appeared to overlap with the 'CCR5 siRNA' panel in Fig. 2B; in addition, the 'Hypoxia / U87‑Mφ' panel in Fig. 1A appeared to overlap with the 'Control siRNA' panel in Fig. 2B. 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; 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 36: 3522‑3528, 2016; DOI: 10.3892/or.2016.5171].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086608","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] Combination of the FGFR4 inhibitor PD173074 and 5‑fluorouracil reduces proliferation and promotes apoptosis in gastric cancer.","authors":"Yan-Wei Ye, Shuang Hu, Ying-Qiang Shi, Xie-Fu Zhang, Ye Zhou, Chun-Lin Zhao, Guo-Jun Wang, Jian-Guo Wen, Hong Zong","doi":"10.3892/or.2025.9004","DOIUrl":"https://doi.org/10.3892/or.2025.9004","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the western blot data shown in Figs. 1E and 4, the FGFR blots and control GAPDH blots were both strikingly similar in these figures, suggesting that the same data had been included in these, even though the results from differently performed experiments were intended to have been portrayed. 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; 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 30: 2777‑2784, 2013; DOI: 10.3892/or.2013.2796].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275271","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":"Induction of immunogenic necroptosis by shikonin in drug‑resistant head and neck squamous cell carcinoma cells.","authors":"Satsuki Kishita, Naoki Umemura, Hiromi Miyazaki, Makoto Adachi, Hideki Yagi, Emika Ohkoshi","doi":"10.3892/or.2025.8996","DOIUrl":"10.3892/or.2025.8996","url":null,"abstract":"<p><p>In recent years, immune checkpoint inhibitors such as nivolumab have been used to treat recurrent or metastatic head and neck cancer. However, some patients do not respond to nivolumab, and the treatment options for these patients are limited. Therefore, identifying compounds for developing new therapeutic strategies for intractable cancer is important. The acquired multidrug‑resistant metastatic head and neck squamous cell carcinoma cell line, R HSC‑3, expresses refractory cancer‑specific proteins such as the drug excretion transporter, ATP binding cassette subfamily G member 2, the cancer stem cell markers, CD44, SRY‑box transcription factor 9 and Notch, and the poor prognosis factor, fibroblast growth factor 9, and is a useful <i>in vitro</i> model for acquired multidrug resistance. In the present study, compounds that may be more effective than conventional chemotherapeutic drugs in R HSC‑3 cells were searched and the cell death mechanism was investigated. The results showed that naphthoquinones inhibited the viability of R HSC‑3 cells at low concentrations and induced necroptotic cell death. Naphthoquinone‑induced necroptotic cell death in R HSC‑3 cells induced the expression of calreticulin, an immunogenic marker. It was further found that mitochondrial‑derived reactive oxygen species mediated the oxidative stress damage by naphthoquinone‑induced necroptotic cell death in these cells. Moreover, necroptotic cell death by shikonin, a naphthoquinone, may generate immunogenic signals from multidrug‑resistant cancer cells. The present study revealed that naphthoquinones may not only induce necroptosis in refractory head and neck cancer cells but also induce tumor immunity. Therefore, naphthoquinones may represent a new avenue for the development of new therapeutic agents targeting multidrug‑resistant head and neck cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12498129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149924","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] TGF‑β1 mediates epithelial to mesenchymal transition via the TGF‑β/Smad pathway in squamous cell carcinoma of the head and neck.","authors":"Changyun Yu, Yong Liu, Donghai Huang, Yaozhang Dai, Gengming Cai, Jinjie Sun, Ting Xu, Yongquan Tian, Xin Zhang","doi":"10.3892/or.2025.9001","DOIUrl":"10.3892/or.2025.9001","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 assay data shown in Fig. 2C and 4D, two pairs of overlapping sections of data were identified comparing the panels in these figures, where the results from differently performed experiments were intended to have been portrayed. The authors were contacted by the Editorial Office to offer an explanation for this apparent duplication of data within the two figures; 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 25: 1581‑1587, 2011; DOI: 10.3892/or.2011.1251].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213299","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":"Hydroxypropyl‑β‑cyclodextrin/thymoquinone inclusion complex inhibits non‑small cell lung cancer progression through NF‑κB‑mediated ferroptosis.","authors":"Wei-Wei Zheng, Jia-Xuan Ding, Yang-Xin Liang, Ling Ye","doi":"10.3892/or.2025.8990","DOIUrl":"10.3892/or.2025.8990","url":null,"abstract":"<p><p>Thymoquinone (TQ) is a quinone isolated from the black seed <i>Nigella sativa</i> and has been extensively investigated in the pharmaceutical field due to its promising therapeutic value. There have been reports on the potential anti‑cancer properties of TQ, whereas the clinical application of TQ is greatly restricted by its low water solubility and poor delivery. In the present study, TQ was encapsulated into hydroxypropyl‑β‑cyclodextrin (HP‑β‑CD) using the freeze‑drying method to form a TQ/HP‑β‑CD inclusion complex. Then, the TQ/HP‑β‑CD inclusion complex was characterized by Fourier transform infrared, differential scanning calorimetry, X‑ray diffraction and scanning electron microscopy. HP‑β‑CD as an excipient significantly enhances the water solubility of TQ, and TQ/HP‑β‑CD demonstrated excellent biocompatibility on normal cells both <i>in vitro</i> and <i>in vivo</i>. Moreover, the complexation with HP‑β‑CD enhanced the anticancer activity of TQ against non‑small cell lung cancer cells and its mechanism of action is related to ferroptosis mediated by NF‑κB. Such an enhanced cytotoxic effect may be attributed to the effective complexation of TQ in HP‑β‑CD, which enhances its water solubility and bioavailability.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086610","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":"REV1‑targeting inhibitor JH‑RE‑06 induces ferroptosis via NCOA4‑mediated ferritinophagy in colorectal cancer cells.","authors":"Jianhua Cheng, Xiaoxia Yang, Wen Zhao, Jie Xu, Yanjie Hao, Fang Xu","doi":"10.3892/or.2025.8992","DOIUrl":"10.3892/or.2025.8992","url":null,"abstract":"<p><p>Oncogenes accelerate DNA replication, leading to the activation of excessive replication origins. This process triggers replication stress (RS) and genomic instability in cancer cells, positioning RS as a promising therapeutic target. Translesion synthesis (TLS) functions as a DNA damage repair bypass mechanism, compensating for RS and conferring a proliferation advantage to cancer cells. Despite its therapeutic potential, the application of the TLS polymerase REV1 (REV1 DNA directed polymerase (REV1) inhibitor JH‑RE‑06 in colorectal cancer (CRC) remains unexplored. Bioinformatics analysis of clinical samples from The Cancer Genome Atlas (TCGA) database demonstrated marked REV1 upregulation in colorectal tumors compared with normal tissues, which was associated with a poorer prognosis. JH‑RE‑06 effectively suppressed CRC tumorigenesis both <i>in vitro</i> and <i>in vivo</i>. Mechanistically, drug rescue experiments and proteomics revealed that cell death triggered by JH‑RE‑06 was associated with elevated oxidative stress and induction of ferroptosis‑associated signaling. Transmission electron microscopy revealed characteristic morphological changes associated with ferroptosis, including a significant reduction in mitochondrial abundance and the presence of autophagic vacuoles containing engulfed mitochondria. Biochemical assays confirmed that JH‑RE‑06 significantly increased intracellular Fe^²+ and malondialdehyde (MDA) levels while reducing glutathione levels, indicative of ferroptosis. Western blot analysis revealed decreased levels of antioxidant proteins, including superoxide dismutase 2 (SOD2) and glutamate‑cysteine ligase catalytic subunit (GCLC), as well as ferritin. Furthermore, western blot and FerroOrange assays, combined with Autophagy‑related Gene 7 (ATG7) and Nuclear Receptor Coactivator 4 (NCOA4) knockdown experiments, demonstrated that JH‑RE‑06 activated ferroptosis in CRC via NCOA4‑mediated ferritinophagy. Safety evaluation via hematoxylin and eosin staining of major organs in mice showed no notable pathological damage induced by JH‑RE‑06. Taken together, these findings establish REV1 as a potential diagnostic biomarker and therapeutic target in CRC. REV1 inhibitor JH‑RE‑06 promoted NCOA4‑mediated ferritinophagy and induced programmed cell death, thereby highlighting its potential as a safe and effective therapeutic strategy for CRC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12485597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150124","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":"Lymphadenectomy in upper tract urothelial carcinoma: Clinical insights and controversies (Review).","authors":"Dihao Lv, Yinglong Huang, Haihao Li, Shi Fu, Chen Gong, Chadanfeng Yang, Jiansong Wang, Haifeng Wang, Zhiyong Tan, Mingxia Ding","doi":"10.3892/or.2025.8970","DOIUrl":"10.3892/or.2025.8970","url":null,"abstract":"<p><p>Upper tract urothelial carcinoma (UTUC), a relatively rare but highly malignant tumor arising from the renal pelvis and the urothelial layer of the ureter, accounts for 5‑10% of all urothelial malignancies. The lack of specific early symptoms commonly results in a delayed diagnosis, with >60% of cases being diagnosed at an advanced stage of the disease. Lymph node involvement can critically affect the clinical outcomes, thus serving as a key prognostic indicator, guiding both staging protocols and treatment strategies. Lymphadenectomy, typically performed alongside radical nephroureterectomy, not only assists in evaluating the extent of the regional metastases, but also plays a critical role in guiding both staging and treatment planning. Although several studies have suggested that a more extensive lymph node dissection (LND) can improve cancer‑specific survival and disease‑free survival rates, there is still no consensus on the optimal extent of dissection or a universally accepted surgical template. The present review aims to summarize the existing evidence on the efficacy of LND in UTUC, thus emphasizing its potential in staging, outcome prediction and possible survival benefits. The review also aims to address the challenges caused by inconsistent LND practices and the limited availability of robust prospective data. Furthermore, it discusses novel biomarkers that could improve patient classification, and proposes future research directions to improve the management of UTUC through more personalized and evidence‑driven LND strategies.</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/PMC12365877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144848191","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] Overexpression of SET oncoprotein is associated with tumor progression and poor prognosis in human gastric cancer.","authors":"Xiaoning Yuan, Te Zhang, Xin Zheng, Yunfei Zhang, Tingting Feng, Pengfei Liu, Zhiting Sun, Shanshan Qin, Xuewen Liu, Liang Zhang, Jie Song, Ying Liu","doi":"10.3892/or.2025.8976","DOIUrl":"10.3892/or.2025.8976","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, the authors contacted the Editor to explain that, concerning the cell invasion assay experiments shown in Fig. 4, and due to an error made in filing the data, the image featured for the OA group / MGC803 cellular experiment in Fig. 4C had been inadvertently duplicated from the invasion image showing the shSET group / SGC7901 cellullar experiment in Fig. 1A. Additionally, a partial overlap was noted between the migration image of the MGC803 cells for the NC siRNA group in Fig. 4D (scratch‑wound assay experiments) and the corresponding image in Fig. 3B. Although both images represent the same cell line with the NC siRNA group, the authors wished to provide a revised version of this data panel in Fig. 4D (in addition to the correction needed for Fig. 4C) for the sake of clarity.  The corrected version of Fig. 4 is shown on the next page. Note that the revisions made to this figure do not affect the overall conclusions reported in the paper, and all the authors agree with the publication of this corrigendum. The authors are grateful to the Editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 38: 1733‑1741, 2017; DOI: 10.3892/or.2017.5788].</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/PMC12402758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963687","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] Lysine demethylase 2A promotes the progression of ovarian cancer by regulating the PI3K pathway and reversing epithelial‑mesenchymal transition.","authors":"Dan-Hua Lu, Jiang Yang, Li-Kun Gao, Jie Min, Jian-Ming Tang, Ming Hu, Yang Li, Su-Ting Li, Jing Chen, Li Hong","doi":"10.3892/or.2025.8971","DOIUrl":"10.3892/or.2025.8971","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that one of the colony‑formation assay images shown in Fig. 2D for the SKOV3 experiments was strikingly similar to the 'SKOV3/0 µM LY294002' image shown in Fig. 5E, if one of the dishes were to be rotated 90°. Upon performing an independent analysis of the data in this paper in the Editorial Office, it also came to light that the data shown for the MMP9 blot (A2780 cell line) in Fig. 4E was strikingly similar to the p‑mTOR blot (again for the A2780 cell line) in Fig. 5B, suggesting that one of these figures had been assembled incorrectly. 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; 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 41: 917‑927, 2019; DOI: 10.3892/or.2018.6888].</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/PMC12376644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144848188","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":"Role of osteopontin in cancer: From pathogenesis to therapeutics (Review).","authors":"Wenli Xu, Zhifei Bi, Li Lu, Fuqiang Feng, Laizhao Chen, Chengwu Zhang","doi":"10.3892/or.2025.8969","DOIUrl":"10.3892/or.2025.8969","url":null,"abstract":"<p><p>Osteopontin (OPN) is an extracellular matrix protein secreted by various types of cells, and serves multiple physiological roles such as modulating bone cell maturation, immune responses, tissue repair and regeneration. Aberrant OPN expression contributes to tumor genesis and development. This indicates that OPN serves a crucial role in tumor genesis and could serve as a potential target for tumor interventions. The present review firstly introduces the molecular structure, receptors and physiological functions of OPN. Subsequently, the present review elaborately addresses the pivotal role served by OPN, and its mechanism in tumor initiation and progression, metastasis, and drug resistance. Furthermore, the present review summarizes currently reported OPN‑based tumor intervention strategies. Lastly, the present review also provides perspectives on how to deepen the insights into the exact role of OPN in tumorigenesis, with the aim of aiding the development of novel strategies for tumor therapeutics. The present review broadens the knowledge regarding the pathophysiological role of OPN, so that novel OPN‑based cancer treatment strategies may be proposed.</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/PMC12365887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799690","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}