International journal of oncology最新文献

{"title":"[Retracted] SRF‑miR‑29b‑MMP2 axis inhibits NSCLC invasion and metastasis.","authors":"Hong-Yan Wang, Yong-Sheng Tu, Jie Long, Hui-Qiu Zhang, Cui-Ling Qi, Xiao-Bin Xie, Shu-Hua Li, Ya-Jie Zhang","doi":"10.3892/ijo.2025.5750","DOIUrl":"10.3892/ijo.2025.5750","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 1A and Fig. 3A and B showing the results of Transwell invasion and migration experiments, the majority of the data panels were identified as having overlapping sections, such that the affected data panels, which were intended to show the results of differently performed experiments, had all apparently been derived from the same original sources. Owing to the large number of duplications of data that have been identified in this paper, the Editor of <i>International Journal of Oncology</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 47: 641‑649, 2015; DOI: 10.3892/ijo.2015.3034].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983593","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] Biological effects of BMP7 on small‑cell lung cancer cells and its bone metastasis.","authors":"Weiwei Shen, Hailin Pang, Bo Xin, Lian Duan, Lili Liu, Helong Zhang","doi":"10.3892/ijo.2025.5757","DOIUrl":"10.3892/ijo.2025.5757","url":null,"abstract":"<p><p>Subsequently to the publication of the above article, the authors contacted the Editorial Office to explain that, for the cell migration and invasion assay experiments shown in Fig. 3 on p. 1358, the same data had inadvertently been selected to show the results of the 'Migration / SBC‑3‑rhBMP7' experiment in Fig. 3A and the 'Invasion / SBC‑5' experiment in Fig. 3B. After re‑examining their original data, the authors have realized that the data were correctly shown for the 'Migration / SBC‑3‑rhBMP7' experiment in Fig. 3A. Therefore, the revised version of Fig. 3, now showing the correct data for the 'Invasion / SBC‑5' experiment in Fig. 3B, is shown on the next page. 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 53: 1354‑1362, 2018; DOI: 10.3892/ijo.2018.4469].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142505","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":"Strategies for neoantigen screening and immunogenicity validation in cancer immunotherapy (Review).","authors":"Hua Feng, Yuanting Jin, Bin Wu","doi":"10.3892/ijo.2025.5749","DOIUrl":"10.3892/ijo.2025.5749","url":null,"abstract":"<p><p>Cancer immunotherapy stimulates and enhances antitumor immune responses to eliminate cancer cells. Neoantigens, which originate from specific mutations within tumor cells, are key targets in cancer immunotherapy. Neoantigens manifest as abnormal peptide fragments or protein segments that are uniquely expressed in tumor cells, making them highly immunogenic. As a result, they activate the immune system, particularly T cell‑mediated immune responses, effectively identifying and eliminating tumor cells. Certain tumor‑associated antigens that are abnormally expressed in normal host proteins in cancer cells are promising targets for immunotherapy. Neoantigens derived from mutated proteins in cancer cells offer true cancer specificity and are often highly immunogenic. Furthermore, most neoantigens are unique to each patient, highlighting the need for personalized treatment strategies. The precise identification and screening of neoantigens are key for improving treatment efficacy and developing individualized therapeutic plans. The neoantigen prediction process involves somatic mutation identification, human leukocyte antigen (HLA) typing, peptide processing and peptide‑HLA binding prediction. The present review summarizes the major current methods used for neoantigen screening, available computational tools and the advantages and limitations of various techniques. Additionally, the present review aimed to summarize experimental strategies for validating the immunogenicity of the predicted neoantigens, which will determine whether these neoantigens can effectively trigger immune responses, as well as challenges encountered during neoantigen screening, providing relevant recommendations for the optimization of neoantigen‑based immunotherapy.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980438","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":"Targeting CALR reduces energy metabolism of esophageal cancer cells and inhibits tumor‑associated fibroblast infiltration.","authors":"Yu Miao, Xiaofei Wang, Fang He, Feixiong Zhang, Ying Huang, Yafang Lai, Yuanzhen Wang, Lina Zhang, Hua Yin, Xiangkun Meng, Hao Liu, Weiqiang Li, Shaoqi Yang","doi":"10.3892/ijo.2025.5755","DOIUrl":"10.3892/ijo.2025.5755","url":null,"abstract":"<p><p>Calreticulin (CALR) supports the induction of dendritic cell maturation, which makes it a key target for effective esophageal squamous cell carcinoma (ESCC) immunotherapy. The mechanism of CALR in the immunotherapy of ESCC is not fully studied. The aim of the present study was to explore the contributing role of CALR in ESCC progression. The association of CALR expression with calnexin (CANX) and protein disulfide isomerase A3 (PDIA3) expression in ESCC was analyzed. The functions of CALR in ESCC cells were examined by detection of cell migration, endoplasmic reticulum (ER) stress, mitochondrial function, cytoskeletal remodeling, cell proliferation and apoptosis. The effects of CALR on tumor growth and tumor‑associated fibroblast infiltration were examined by subcutaneous xenograft assay. The expression of CALR, CANX and PDIA3 in ESCC tissue significantly increased and the expression of PDIA3 was positively associated with CANX. Overexpression of CALR resulted in enhanced cell proliferation, migration, ER stress, mitochondrial function and cytoskeletal remodeling; knockdown of CALR expression had the opposite effect. In the subcutaneous xenograft assay, knockdown CALR significantly inhibited the growth of esophageal cancer tumors, suppressed the invasion of tumor‑associated fibroblasts and decreased the expression of α‑smooth muscle actin (α‑SMA), fibroblast activation protein (FAP), fibroblast specific protein‑1 (FSP1), platelet‑derived growth factor and transforming growth factor beta (TGF‑β) in tumor tissue. These findings suggested that CALR promotes the progression of ESCC by regulating ER stress and mitochondrial function to mediate ATP production, cytoskeletal remodeling, cell proliferation and apoptosis through CANX and PDIA3. Knockdown CALR significantly inhibited tumor‑associated fibroblast infiltration and is a potential drug target for ESCC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142589","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":"Chaetocin enhances tumor necrosis factor‑related apoptosis‑inducing ligand‑mediated apoptosis by enhancing DR5 stabilization and reactive oxygen species generation in human glioblastoma cells.","authors":"Hui-Jung Jung, Jin Kyung Kim, Seong-Il Suh, Won-Ki Baek","doi":"10.3892/ijo.2025.5753","DOIUrl":"10.3892/ijo.2025.5753","url":null,"abstract":"<p><p>Chaetocin, a fungal metabolite, exerts notable antiproliferative effects against solid tumors by triggering apoptosis; however, the mechanisms underlying its effects remain unclear. As tumor necrosis factor (TNF)‑related apoptosis‑inducing ligand (TRAIL) promotes apoptosis in certain types of tumor, the present study aimed to explore the sensitizing effects of chaetocin in TRAIL‑induced apoptosis in human glioblastoma cells and the underlying mechanism. Human glioblastoma cells (U343MG, U87MG, U251MG, and T98G) and embryonic kidney cells (HEK293) were co‑treated with chaetocin and TRAIL, followed by assessment of cell viability. The results from viability and apoptosis assays demonstrated a significant increase in caspase-dependent apoptosis in glioblastoma cells, but not in HEK293 cells, upon co-treatment with chaetocin and TRAIL. Additionally, death receptor 5 (DR5) expression analysis demonstrated that co‑treatment with chaetocin and TRAIL upregulated DR5 expression in a dose‑ and time‑dependent manner by increasing the stability of DR5 on the cell surface. In glioblastoma cells, small interfering RNA‑mediated DR5 knockdown markedly suppressed chaetocin/TRAIL‑induced apoptosis. Moreover, chaetocin enhanced reactive oxygen species (ROS) production, which facilitated TRAIL‑mediated apoptosis by enhancing DR5 upregulation. Thus, chaetocin sensitized the human glioblastoma cell lines U87MG and T98G to TRAIL‑mediated apoptosis by upregulating DR5 expression through ROS-mediated mechanisms. The present findings underscore chaetocin as a potential novel therapeutic agent for glioblastoma.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077962","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":"Multifaceted roles of lactate dehydrogenase in liver cancer (Review).","authors":"Hai Jin, Qian Liu, Jin Li, Siyu Zhao, Biguang Tuo","doi":"10.3892/ijo.2025.5756","DOIUrl":"10.3892/ijo.2025.5756","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) has high morbidity and mortality rates, and metabolic reprogramming of HCC cells supports the proliferation and development of tumor cells. Lactate dehydrogenase (LDH), a key metabolic enzyme, can maintain the rapid proliferative demand of tumor cells by promoting glycolysis and lactate production in HCC cells. In addition, LDH regulates redox homeostasis and influences lipid synthesis and signaling pathways, further promoting tumor invasion and metastasis. In the tumor microenvironment, LDH affects the function of immune cells and stromal cells by regulating the lactate concentration in and promoting the immune escape and angiogenesis of tumor cells. Since elevated levels of LDH are closely associated with tumor load, invasiveness and poor prognosis, LDH also has promising applications in the early diagnosis, treatment and prognostic assessment of HCC. The present study reviewed the roles of LDH in the occurrence, development, diagnosis, prognosis and treatment of HCC and explored its value as an important biomarker and potential therapeutic target, with the aim of providing a comprehensive reference for HCC‑related research and clinical practice.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142454","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] Notch1 induces epithelial‑mesenchymal transition and the cancer stem cell phenotype in breast cancer cells and STAT3 plays a key role.","authors":"Xiaojin Zhang, Xiaoai Zhao, Shan Shao, Xiaoxiao Zuo, Qian Ning, Minna Luo, Shanzhi Gu, Xinhan Zhao","doi":"10.3892/ijo.2025.5752","DOIUrl":"10.3892/ijo.2025.5752","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 3A and B on p. 1145 showing the results of cell invasion and migration experiments, four pairs of overlapping data panels were identified, affecting half the panels shown in the figure, such that these data panels, which were intended to show the results of differently performed experiments, had all apparently been derived from the same original source. Owing to the large number of duplications of data that have been identified in this paper, the Editor of <i>International Journal of Oncology</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 46: 1141‑1148, 2015; DOI: 10.3892/ijo.2014.2809].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077958","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":"Targeting the cuproptosis‑associated gene COL22A1 in glioblastoma using EMD‑1204831 and kaempferol.","authors":"Yi Chen, Ye Zhang, Huilan Yang, Qiang Liu, Rui Sui, Ji Shi, Haiyang Liang, Jia Liu, Huizhe Xu, Haozhe Piao","doi":"10.3892/ijo.2025.5744","DOIUrl":"https://doi.org/10.3892/ijo.2025.5744","url":null,"abstract":"<p><p>Glioblastoma (GBM) is a disease with high morbidity and poor prognosis. The combination of traditional Chinese and Western medicine and cuproptosis are known to serve important roles in the treatment of GBM. However, targeting cuproptosis to treat GBM by combining traditional Chinese and Western medicine has not been extensively investigated. Therefore, the present study focused on the diagnosis and treatment of GBM based on cuproptosis. Through a bioinformatics approach, a cuproptosis‑related prognostic model was first constructed. Next, this prognostic model was found to be closely related to immune infiltration, DNA mutation and DNA methylation through multi‑omics analysis. The present study indicated the cell clusters in GBM tissues and the risk scores in each cluster based on single‑cell sequencing data derived from Gene Expression Omnibus. Notably, by screening the CellMiner database, EMD‑1204831 was found to exhibit a high correlation with the risk score. Next, through network pharmacology and molecular docking analysis, the risk score‑related gene collagen type XXII α1 chain (COL22A1) was identified as the target of kaempferol, which is the active component of Ginseng. Notably, kaempferol could decrease the proliferation of GBM cells by inhibiting COL22A1 expression in cell experiments. Finally, kaempferol and EMD‑1204831 had an obvious inhibitory effect on the growth of GBM and sensitized GBM to cuproptosis inducers via COL22A1 in cell and animal experiments. Overall, the present study revealed a cuproptosis‑related combined regimen for GBM.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987694","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] Promoter methylation of RASSF1A modulates the effect of the microtubule‑targeting agent docetaxel in breast cancer.","authors":"Eun Young Gil, Uk Hyun Jo, Hoiseon Jeong, Young Mi Whang, Ok Hee Woo, Kyu Ran Cho, Jae Hong Seo, Aeree Kim, Eun Sook Lee, Insong Koh, Yeul Hong Kim, Kyong Hwa Park","doi":"10.3892/ijo.2025.5745","DOIUrl":"https://doi.org/10.3892/ijo.2025.5745","url":null,"abstract":"<p><p>Following the publication of this paper, and a corrigendum that was subsequently published to take account of anomalies that were identified with the assembly of western blot data in Fig. 5B (doi: 10.3892/ijo.2017.3900), a concerned reader drew to the Editor's attention that, regrettably, there remained possible issues with the duplication of data in the revised version of Fig. 5 provided by the authors in the Corrigendum; in addition, potential anomalies were also noted with the western blot assay data in the originally published versions of Fig. 2A and B. After having performed an independent review of the data in these figures in the Editorial Office, the concerns of the reader were found to be validated. Therefore, the Editor of <i>International Journal of Oncology</i> has decided that this paper should now 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. [International Journal of Oncology 41: 611‑620, 2012; DOI: 10.3892/ijo.2012.1470].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995510","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] lncRNA PLAC2 activated by H3K27 acetylation promotes cell proliferation and invasion via the activation of Wnt/β‑catenin pathway in oral squamous cell carcinoma.","authors":"Fubo Chen, Shengcai Qi, Xu Zhang, Jinjin Wu, Xi Yang, Raorao Wang","doi":"10.3892/ijo.2025.5743","DOIUrl":"10.3892/ijo.2025.5743","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the immunofluorescence assay data shown in Figs. 3C on p. 1189 and 4E on p. 1190 were strikingly similar to data appearing in different form in another pair of articles written by different authors at different research institutes that had already been published elsewhere prior to the submission of this paper to <i>International Journal of Oncology</i>. Given that the abovementioned data had already apparently been published previously, the Editor of <i>International Journal of Oncology</i> has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 54: 1183-1194, 2019; DOI: 10.3892/ijo.2019.4707].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"66 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780067","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}