International journal of oncology最新文献

{"title":"[Expression of Concern] Halofuginone induces the apoptosis of breast cancer cells and inhibits migration via downregulation of matrix metalloproteinase‑9.","authors":"Mei Ling Jin, Sun Young Park, Young Hun Kim, Geuntae Park, Sang Joon Lee","doi":"10.3892/ijo.2025.5812","DOIUrl":"10.3892/ijo.2025.5812","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 cell invasion assay experiments shown in Fig. 4B, the 'Con' and 'LPA+HF' data panels contained an overlapping section, such that data which were intended to show the results of differently performed experiments appeared to have been derived from the same original source. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly 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 continues to investigate this matter further.  [International Journal of Oncology 44: 309‑318, 2014; DOI: 10.3892/ijo.2013.2157].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12551992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307904","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":"Exosomal microRNAs: A new role in the diagnosis and treatment of lung cancer metastases (Review).","authors":"Xin Li, Jian Wang, Weipeng Ge, Xinbo Chen","doi":"10.3892/ijo.2025.5807","DOIUrl":"10.3892/ijo.2025.5807","url":null,"abstract":"<p><p>Lung cancer (LC) is a lethal malignancy that can pose a serious risk to a patient's health. Tumor metastasis is associated with a shorter survival and poor therapeutic outcomes. Epithelial‑mesenchymal transition, cell proliferation and angiogenesis are the key drivers of metastasis, which accounts for cancer malignancy. Exosomal microRNAs (miRNAs) are miRNAs packed and released in exosomes. Exosomal miRNAs promote the metastasis of LC. As the amount and type of exosomal miRNAs are disrupted in pathological situations, they may serve as markers for the diagnosis and treatment of LC. The present review summarizes the effects and underlying mechanisms of exosomal miRNAs in LC metastasis. It also provides an overview of the potential of exosomal miRNAs as diagnostic indicators and therapeutic targets for LC metastasis, highlighting novel avenues for future tailored therapies.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12532287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274411","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] miR‑135b, upregulated in breast cancer, promotes cell growth and disrupts the cell cycle by regulating LATS2.","authors":"Kaiyao Hua, Jiali Jin, Junyong Zhao, Jialu Song, Hongming Song, Dengfeng Li, Niraj Maskey, Bingkun Zhao, Chenyang Wu, Hui Xu, Lin Fang","doi":"10.3892/ijo.2025.5802","DOIUrl":"10.3892/ijo.2025.5802","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 scratch‑wound assay data shown in Fig. 4A, the '24 h/MCF‑7/mir‑135b inhibitor' data panel looked strikingly similar to the '24 h/MCF‑7/NC' data panel in Fig. 10C, albeit the panels were featured rotated through 180° with respect to each other. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly 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 continues to investigate this matter further. [International Journal of Oncology 48: 1997‑2006, 2016; DOI: 10.3892/ijo.2016.3405].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12543313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086234","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":"ZBTB20 promotes ferroptosis through inhibiting TMEM109 expression in glioblastoma cells.","authors":"Xuhao Chen, Mingqi Luo, Xiaoyu Niu, Wang Wang, Huanhuan Cao, Liwei Zhang, Ruolun Wei, Ping Duan","doi":"10.3892/ijo.2025.5803","DOIUrl":"10.3892/ijo.2025.5803","url":null,"abstract":"<p><p>Ferroptosis is an iron‑dependent type of regulated cell death which is dysregulated in several tumors, including glioblastoma (GBM). Zinc finger and BTB domain‑containing protein 20 (<i>ZBTB20</i>), a transcription repressor, is expressed at low levels in GBM and suppresses GBM cell proliferation through the ERK signaling pathway. However, the effect of <i>ZBTB20</i> on ferroptosis has not been explored. The present study aimed to explore the role of ZBTB20 in ferroptosis of glioma cells and its underlying mechanism. The present study demonstrated that both <i>ZBTB20</i> expression and ferroptosis levels in GBM cells were lower than that in normal glial cells. Gain‑ and loss‑of‑function experiments revealed that <i>ZBTB20</i> overexpression promoted ferroptosis and <i>ZBTB20</i> knockdown inhibited ferroptosis in GBM cells. Moreover, the results demonstrated that <i>ZBTB20</i> transcriptionally repressed the expression of transmembrane protein 109 (<i>TMEM109</i>) in GBM cells, assessed using dual‑luciferase reporter and chromatin immunoprecipitation assays. TMEM109 is mainly localized on the endoplasmic reticulum (ER) membrane of cells and regulates calcium leakage at the ER or sarcoplasmic reticulum. The present study revealed that <i>TMEM109</i> overexpression inhibited ferroptosis and <i>TMEM109</i> knockdown promoted ferroptosis in GBM cells. Using co‑transfection experiments, it was further revealed that the promotive effect of <i>ZBTB20</i> can reverse the inhibitory effect of TMEM109 on ferroptosis. In conclusion, the findings indicated that <i>ZBTB20</i> promotes ferroptosis in GBM cells through transcriptionally repressing the expression of <i>TMEM109</i>.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12543314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148879","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] Podoplanin‑mediated TGF‑β‑induced epithelial-mesen-chymal transition and its correlation with bHLH transcription factor DEC in TE‑11 cells.","authors":"Yunyan Wu, Qiang Liu, Xu Yan, Yukio Kato, Makiko Tanaka, Sadaki Inokuchi, Tadashi Yoshizawa, Satoko Morohashi, Hiroshi Kijima","doi":"10.3892/ijo.2025.5805","DOIUrl":"10.3892/ijo.2025.5805","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 scratch‑wound assay experiments shown in Fig. 6 on p. 2318, the 'control siRNA/24 h' and 'podoplanin siRNA/48 h' panels contained an overlapping section of data; such that these data, which were intended to show the results from differently performed experiments, appeared to have been derived from the same original source. Upon analyzing the data independently in the Editorial Office, it came to light that, in addition to control blots, the podoplanin blots were duplicated in Fig. 2A and B, and also in Fig. 3A and B, although it wasn't clear whether this was simply the way in which the authors had chosen to arrange the data in these figures, as the reported experimental conditions were the same in the respective figure parts. The authors were contacted by the Editorial Office to offer an explanation for these possible 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 48: 2310‑2320, 2016; DOI: 10.3892/ijo.2016.3445].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12543312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148908","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] miR‑221/222 promote malignant progression of glioma through activation of the Akt pathway.","authors":"Junxia Zhang, Lei Han, Youlin Ge, Xuan Zhou, Anling Zhang, Chunzhi Zhang, Yue Zhong, Yongping You, Eiyu Pu, Chunsheng Kang","doi":"10.3892/ijo.2025.5808","DOIUrl":"10.3892/ijo.2025.5808","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the Editor's attention that, for the immuno-histochemistry images shown in Fig. 6, the Control/PCNA and Control/p27kip1 panels appeared to be duplicates of each other, where the results of differently performed experiments were intended to have been portrayed. The authors were contacted by the Editorial Office to offer an explanation for this potential anomaly 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 continues to investigate this matter further. [International Journal of Oncology 36: 913‑920, 2010; DOI: 10.3892/ijo_00000570].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12543311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274489","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":"Adipocyte‑derived extracellular vesicles sustain mitochondrial metabolism in breast cancer cells: New insights into the cross‑talk between cancer cells and the tumor microenvironment.","authors":"Luca Gelsomino, Piercarlo Del Console, Maria Stella Murfuni, Marco Gaspari, Francesca Giordano, Giuseppina Daniela Naimo, Marco Fiorillo, Grazia Arpino, Mario Giuliano, Salvatore Panza, Daniela Bonofiglio, Sebastiano Andò, Ines Barone, Cinzia Giordano, Stefania Catalano","doi":"10.3892/ijo.2025.5806","DOIUrl":"10.3892/ijo.2025.5806","url":null,"abstract":"<p><p>Adipocytes represent the most prominent component of breast tissue stroma and are recognized as significant contributors to the observed association between obesity and breast cancer (BC). It has been widely reported that dysfunctional adipose tissue in obesity has a profound effect on the biology of BC via the secretion of several bioactive molecules. Recently, extracellular vesicles (EVs), a heterogeneous group of membrane‑enclosed structures, have been recognized as key players in adipocyte‑BC cell communication. We previously demonstrated that adipocyte‑derived EVs promoted BC proliferation, migration, invasion, stemness and traits of epithelial‑to‑mesenchymal transition through the activation of hypoxia inducible factor‑1α (HIF‑1α). The present study, to further understand the impact of EVs in breast adiponcosis, investigated the effects of adipocyte‑derived EVs on the BC proteome. By employing liquid chromatography‑tandem mass spectrometry and different bioinformatic tools (such as Proteomap, STRING, FunRich, Reactome and MsigDB), it was found that adipocyte‑derived EVs regulated the expression of multiple proteins implicated in metabolic processes. Adipocyte‑derived EVs shifted cell metabolism towards oxidative phosphorylation in estrogen receptor‑positive (ER+) BC cell lines, including MCF‑7, ZR‑75‑1 and BT‑474 BC cells, through an increased mitochondrial activity along with an enhanced ATP production. These findings were extended by treating BC cells with EVs isolated from the serum of patients with BC classified as normal weight (NW‑EVs) and overweight or obese (OW/Ob‑EVs). Treatment of BC cells with OW/Ob‑EVs resulted in a significant increase of mitochondrial activity and ATP production compared with NW‑EVs. Of note, inhibition of HIF‑1α expression/activity reversed the effects of both adipocyte‑derived EVs and OW/Ob‑EVs on BC cell metabolism. In conclusion, the present study underscored the pivotal role of EVs in the BC‑obesity link, highlighting their involvement in driving metabolic reprogramming in ER+ BC cells through HIF‑1α.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"67 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12543315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274409","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 metabolic reprogramming of cancer‑associated fibroblasts in tumor development and progression (Review).","authors":"Ruyue Li, Yintao Li","doi":"10.3892/ijo.2025.5796","DOIUrl":"10.3892/ijo.2025.5796","url":null,"abstract":"<p><p>The occurrence and development of tumors is affected by tumor cells themselves and various components of the tumor microenvironment (TME). Among these, cancer‑associated fibroblasts (CAFs), the main stromal component, can differentiate from different cell types and play an important role in the TME. The present review summarized the role of the metabolic reprogramming of CAFs in tumor development and progression. As the rapid growth of tumors is a process inseparable from energy supply and the TME is characterized by hypoxia and nutrient deficiencies, metabolic reprogramming can reverse the effects of a lack of energy supply in the TME. Studies have found that CAFs can affect tumor proliferation, migration, invasion, metastasis and drug resistance by changing metabolic patterns. The present review promoted research on the metabolic reprogramming of CAFs and emphasized the importance of considering the heterogeneity and plasticity of CAFs in the TME, which will lead to the development of more effective therapeutic strategies that target specific metabolic pathways in CAFs, potentially improving the efficacy of cancer treatments and overcoming drug resistance.</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/PMC12425346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953961","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":"Progerin regulates actin cytoskeletal remodeling and inhibits EMT and metastasis in triple‑negative breast cancer cells.","authors":"Xinxian Huang, Weizhao Luo, Weixian Liu, Xinguang Liu, Weichun Chen","doi":"10.3892/ijo.2025.5798","DOIUrl":"10.3892/ijo.2025.5798","url":null,"abstract":"<p><p>Triple‑negative breast cancer (TNBC) is a subtype of breast cancer, known for its poor prognosis due to its high invasiveness, strong metastatic tendencies and propensity for recurrence. Epithelial to mesenchymal transition (EMT) is a crucial process in tumor invasion and metastasis and in the formation of cancer‑initiating cells. Hutchinson‑Gilford progeria is a rare condition characterized by accelerated aging, caused by a mutated form of lamin A, known as progerin. The present study aimed to investigate the effect of progerin overexpression on TNBC and uncover its underlying mechanisms of action. Therefore, cell senescence was assessed using senescence‑associated β‑galactosidase staining, while cell proliferation was measured by colony formation, Cell Counting Kit‑8 and EdU assays. Additionally, cell metastasis was evaluated using wound‑healing, Transwell and cell adhesion assays. Immunofluorescence staining was carried out to observe actin cytoskeleton and nuclear morphology. The results showed that progerin markedly suppressed the colony formation, migration, invasion and adhesion abilities of BT‑549 and MDA‑MB‑231 TNBC cell lines, without affecting cell senescence or proliferation. In addition, progerin overexpression altered nuclear morphology and actin cytoskeleton organization in TNBC cells. Furthermore, the expression levels of the mesenchymal markers, N‑cadherin, vimentin, Snail and Slug, were reduced, while those of the epithelial marker, E‑cadherin, were enhanced in TNBC cells. Overall, the results of the present study suggested that progerin overexpression could inhibit TNBC cell metastasis, probably via actin cytoskeleton remodeling and regulate the expression levels of the cytoskeletal‑related proteins, anillin and β‑catenin, and those of the EMT‑related ones. The aforementioned findings could provide novel insights into the identification of potential molecular targets for breast cancer therapy.</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/PMC12456472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040082","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":"Potential of Fibulin2 as a therapeutic target against cancer and as a diagnostic marker (Review).","authors":"Yongqiang Yang, Zi Wang, Lian Weng, Jun Fei, Zhong Li","doi":"10.3892/ijo.2025.5799","DOIUrl":"10.3892/ijo.2025.5799","url":null,"abstract":"<p><p>Cancers are not merely composed of tumor cells; rather, they constitute a complex tumor microenvironment (TME) comprising diverse cell types and noncellular factors. Extracellular matrix (ECM) represents a critical component of the TME. Fibulin2 participates in ECM formation in various tumors, and its altered expression in multiple malignancies can affect tumor cell proliferation and invasiveness. Additionally, Fibulin2 has emerged as a potential biomarker in various cancer types and serves a pivotal role in tumor progression. Consequently, therapeutic strategies targeting Fibulin2 hold considerable promise. However, the research and development of Fibulin2‑targeted therapeutics has progressed at a relatively slow pace. Therefore, the roles and mechanisms of Fibulin2 in various malignancies, along with investigations into its utility as a biomarker, are comprehensively discussed in the present review. This may provide valuable guidance for the clinical translation and application of Fibulin2‑targeted therapies, and the utilization of Fibulin2 as a predictive biomarker.</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/PMC12456471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040112","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}