International journal of oncology最新文献

{"title":"Emerging agents that target signaling pathways in cancer fibroblast cells (Review).","authors":"Yan Wan, Xiang-Qing Liu, Dong Liu, Ke-Di Li, Dan-Dan Zhang","doi":"10.3892/ijo.2026.5900","DOIUrl":"10.3892/ijo.2026.5900","url":null,"abstract":"<p><p>Cancer‑associated fibroblasts (CAFs) play a critical role in cancer development, recurrence and metastasis. Several signaling pathways are crucial in CAF development, including fibroblast activation protein (FAP), phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR), Janus kinase/signal transducers and activators of transcription (JAK/STAT), nuclear factor κB (NF‑κB), transforming growth factor β (TGF‑β), ferroptosis, apoptosis and autophagy pathways. Targeting the ferroptosis signaling pathway specifically kills CAFs. Therefore, targeting these pathways may inhibit the protumorigenic functions of CAFs. Small molecule drugs, due to their well‑dispersed spatial structures and distinct chemical properties, exhibit promising druggability and pharmacokinetic profiles. These characteristics make small molecule drugs highly advantageous in drug development and increasingly favored in the market. The present review summarized current studies on small molecule compounds that inhibit CAF progression, encompassing inhibitors of the PI3K/AKT/mTOR, JAK/STAT, TGF‑β and NF‑κB pathways, as well as activators of the FAP, ferroptosis, apoptosis and autophagy pathways. These small molecule compounds underscore the significance of CAFs in tumor progression and suggest novel strategies for cancer treatment by targeting CAFs in clinical settings.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148163141","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] Radiation‑inducible silencing of uPA and uPAR <i>in vitro</i> and <i>in vivo</i> in meningioma.","authors":"Venkateswara Rao Gogineni, Arun Kumar Nalla, Reshu Gupta, Bharathi Gorantla, Meena Gujrati, Dzung H Dinh, Jasti S Rao","doi":"10.3892/ijo.2026.5890","DOIUrl":"10.3892/ijo.2026.5890","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 immunocytochemical and immunohistochemical experiments shown in Fig. 5A‑C on p. 815, several of the data panels exhibited overlapping sections, such that the data shown in the affected panels had all apparently been derived from the same original sources. Owing to the large number of duplications of data that were 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 36: 809‑816, 2010; DOI: 10.3892/ijo_00000557].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948415","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":"Metabolic remodeling by circular RNAs in gastric tumorigenesis: From mechanisms to biomarker discovery (Review).","authors":"Xinyi Liang, Tianlin Wang, Jiale Ma, Shuangmei Zhao, Wang Gao, Yan Yang, Xinyuan Zhang, Huizhen Li","doi":"10.3892/ijo.2026.5899","DOIUrl":"10.3892/ijo.2026.5899","url":null,"abstract":"<p><p>Gastric cancer (GC), which primarily originates from gastric mucosal epithelium, is driven by factors such as <i>Helicobacter pylori</i> infection, genetic susceptibility and lifestyle. GC poses a serious threat to patient survival and quality of life. Metabolic reprogramming, a hallmark of tumorigenesis and progression, enables cancer cells to continuously adapt their energy metabolism to support proliferation, invasion, metastasis and drug resistance. Circular RNAs (circRNAs) are a class of non‑coding RNAs characterized by a covalently closed circular structure, which confers high stability. They are differentially expressed in tumor cells and facilitate tumor proliferation and metastasis through multiple mechanisms such as microRNA sponging, protein binding, short peptide translation and N⁶‑methyladenosine modification. Furthermore, circRNAs contribute to tumor metabolic remodeling, meeting the energy demands of tumor cells by regulating key enzymes and transporters involved in metabolic pathways, thereby modulating the synthesis or degradation of metabolites. The present review summarizes the mechanisms by which circRNAs mediate different metabolic modes during the initiation and progression of GC as well as discusses their potential as biomarkers for GC. By systematically elucidating the intricate interactions between circRNAs and metabolic reprogramming in GC, the present study aims to provide a theoretical foundation for the development of innovative therapeutic strategies against GC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148163183","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":"BMP4 derived from human gastrointestinal carcinoma cells impairs myogenic differentiation: A possible <i>in vitro</i> mechanism of cancer‑induced cachexia.","authors":"Kazuki Higure, Yoshihiko Kitajima, Naoya Kimura, Shota Ikeda, Shohei Matsufuji, Tomokazu Tanaka, Hirokazu Noshiro","doi":"10.3892/ijo.2026.5891","DOIUrl":"10.3892/ijo.2026.5891","url":null,"abstract":"<p><p>Gastrointestinal cancer (GIC) frequently causes cancer cachexia, the major feature of which is the loss of skeletal muscle mass. The degradation of muscular proteins by cancer‑derived factors in the major pathogenesis of cancer‑induced muscle wasting is a known phenomenon. However, this mechanism has mainly been demonstrated using rodent cancer cells, and it may not always be applicable to human cancer types. Impaired skeletal muscle differentiation and regeneration have attracted attention as alternative inducers of cancer cachexia. The present study revealed that conditioned medium from four human GIC cell lines inhibited C2C12 myoblast differentiation by inducing the expression of the inhibitor of DNA binding (Id) proteins Id1 and Id3, which mediated via bone morphogenetic protein (BMP)‑Smad signaling. The results suggested that BMP‑Smad1/5/8‑Id signaling inhibited the expression of a MRF member, myogenin and its downstream myogenic genes, thus leading to unsuccessful differentiation into myotubes. Furthermore, the present study identified high levels of BMP4 secretion from these four human GIC cell lines and demonstrated that an inhibitor of BMP receptor, dorsomorphin or abrogation of BMP4 by siRNA in the GIC cells restored myogenic differentiation in C2C12 cells. The present study uncovered, for the first time, that BMP4 derived from human GIC cells exogenously inhibited myoblast differentiation by activating the Smad1/5/8‑Id signaling axis. In the future, this <i>in vitro</i> study may help to elucidate the complicated mechanisms underlying cancer‑induced cachexia in humans.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948429","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":"snoRNAs and their derived sdRNAs: Emerging regulators, biomarkers, and therapeutic targets in human cancers (Review).","authors":"Jiahui Mao, Hao Lin, Feng Gu, Zhaoji Pan","doi":"10.3892/ijo.2026.5893","DOIUrl":"10.3892/ijo.2026.5893","url":null,"abstract":"<p><p>Small nucleolar RNAs (snoRNAs) are a conserved class of non‑coding RNAs that guide 2'‑O‑methylation and pseudouridylation of ribosomal RNA. First identified over five decades ago, snoRNAs have emerged as critical regulators of cellular function, with high‑throughput sequencing revealing their dysregulation in numerous human diseases, particularly cancer. In the present review, the biogenesis, classification, and modification mechanisms of snoRNAs and snoRNA‑derived fragments (sdRNAs) are comprehensively summarized. Recent advances in understanding their non‑canonical functions are highlighted, which extend beyond ribosomal RNA modification to include regulation of mRNA splicing, stability, and protein interactions. These diverse mechanisms enable snoRNAs to influence key cancer‑related processes such as proliferation, metastasis, metabolic reprogramming, and therapy resistance. A comprehensive overview of snoRNA dysregulation across major cancer types is provided, including colorectal, hepatocellular, gastric, lung, breast, and ovarian cancers, with a detailed discussion of underlying molecular pathways. Furthermore, their emerging potential as diagnostic and prognostic biomarkers detectable in liquid biopsies is examined, as well as their promise as therapeutic targets amenable to antisense oligonucleotide and small molecule intervention. The present review integrates current knowledge of snoRNA/sdRNA biology and highlights critical gaps and future directions, providing a foundation for translating these regulatory RNAs into clinical oncology applications.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948543","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] Semaphorin 5A suppresses the proliferation and migration of lung adenocarcinoma cells.","authors":"Pin-Hao Ko, Govinda Lenka, Yu-An Chen, Eric Y Chuang, Mong-Hsun Tsai, Yuh-Pyng Sher, Liang-Chuan Lai","doi":"10.3892/ijo.2026.5894","DOIUrl":"10.3892/ijo.2026.5894","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 Fig. 1, showing that the downregulation of SEMA5A in lung adenocarcinoma tissues is associated with poor overall survival, was strikingly similar to a figure that had previously appeared in an article by Dan Wang and colleagues in <i>American Journal of BioMedicine</i> in 2014 (doi: 10.18081/2333‑5106/014‑03/292‑305). Upon receiving notification of this issue, the authors identified that Fig. 1, as shown, had been included in this paper erroneously, and requested that a corrigendum be published, featuring the correct data for Fig. 1. However, after carefully considering the matter, the Editor of <i>International Journal of Oncology</i> has decided that this paper should instead be retracted from the Journal on account of a lack of confidence in the presented data. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 56: 165‑177, 2020; DOI: 10.3892/ijo.2019.4932].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147987559","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] Histone deacetylase inhibitors induce in human hepatoma HepG2 cells acetylation of p53 and histones in correlation with apoptotic effects.","authors":"D Carlisi, B Vassallo, M Lauricella, S Emanuele, A D'anneo, E Di Leonardo, P Di Fazio, R Vento, G Tesoriere","doi":"10.3892/ijo.2026.5896","DOIUrl":"10.3892/ijo.2026.5896","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 blot analyses shown in Fig. 2A and B on p. 179, the control β‑actin blots in Fig. 2A were very similar to a section of the control blots in Fig. 2B, albeit with some horizontal and vertical resizing of the bands in question, even though the affected lanes of the gel highlighted different experimental treatments. 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, and we are awaiting their response. 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 32: 177‑184, 2008; DOI: 10.3892/ijo.32.1.177].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147987537","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":"Deubiquitinating enzymes in cervical cancer: Molecular mechanisms and therapeutic implications (Review).","authors":"Chang-Zhu Pei, Xiao-Xing Song, Hao Xu, Kwang-Hyun Baek","doi":"10.3892/ijo.2026.5892","DOIUrl":"10.3892/ijo.2026.5892","url":null,"abstract":"<p><p>Cervical cancer (CC) remains a major global gynecological malignancy, with a rising incidence among younger women in specific regions. Human papillomavirus (HPV) screening and cytological examination have markedly reduced the disease burden; nonetheless, tumor progression, therapeutic resistance and recurrence continue to pose major clinical challenges. Thus, elucidating the molecular mechanisms underlying the progression of CC is crucial. Deubiquitinating enzymes (DUBs) regulate ubiquitin‑dependent protein turnover and signaling, emerging as vital modulators of cell cycle progression, DNA damage response, apoptosis, immune regulation and HPV‑associated carcinogenesis. Notably, DUBs facilitate CC progression by stabilizing oncogenic proteins, regulating tumor suppressors and modulating major signaling pathways. In addition, several DUBs are closely associated with radiosensitivity, chemoresistance and potential targeted therapeutic strategies. The present review summarizes the molecular mechanisms and therapeutic implications of DUBs in CC, while discussing their translational value for future clinical applications.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948497","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":"Circulating proteins as biomarkers of response to cancer immunotherapy (Review).","authors":"Celeste Pinard, Angeline Ginzac, Catherine Abrial, Xavier Durando, Nina Radosevic-Robin","doi":"10.3892/ijo.2026.5889","DOIUrl":"10.3892/ijo.2026.5889","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have revolutionized cancer management; however, durable benefit is observed only in a minority of patients. To overcome the limitations of currently approved tumour tissue‑based biomarkers of response, several approaches based on liquid biopsy are currently being developed. Among them, circulating proteins, such as soluble immune checkpoint regulators, cytokines, chemokines, growth factors and cellular modulators, are being increasingly assessed by multiplex technologies that use a low volume of biofluids and offer rapid results. Serum/plasma programmed death‑ligand 1, cytotoxic t‑lymphocyte‑associated protein 4, T‑cell immunoglobulin and mucin‑domain containing‑3, lymphocyte activation gene‑3, interleukin (IL)‑6 and IL‑8 have emerged as potentially useful indicators of early response or resistance to ICIs, particularly when quantified during treatment. However, the optimal timing of on‑treatment blood sampling remains to be determined. The current review aimed to present the most important findings on the association between circulating proteins and response to ICIs in solid tumours, and to discuss the position of this biomarker class in the current landscape of biomarkers for ICI therapy.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837685","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":"Integrin beta 4 promotes colorectal cancer progression by upregulating Ezrin and activating the Wnt/β‑catenin signaling pathway.","authors":"Jing Wang, Yi Si, Mingda Xuan, Shuangshuang Han, Kunyi Liu, Jiao Jiao, Xiaoyan Men, Hongfei Li, Jia Wang, Ting Liu, Weifang Yu","doi":"10.3892/ijo.2026.5895","DOIUrl":"10.3892/ijo.2026.5895","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a major cause of cancer‑related mortality worldwide. Integrin beta 4 (ITGB4) has been previously identified as being overexpressed in CRC; however, its precise oncogenic mechanism remains unclear. The present study aimed to elucidate the functional role of ITGB4 in CRC progression and identify its downstream molecular effectors to provide new insights for targeted therapy. The biological functions of ITGB4 were investigated in CRC cell lines (SW480 and HCT116) using a series of <i>in vitro</i> assays, including Cell Counting Kit‑8, colony formation, Transwell migration and invasion, and flow cytometry for apoptosis following ITGB4 knockdown. An <i>in vivo</i> xenograft mouse model was used to evaluate the effect of ITGB4 on tumor growth. Downstream targets were screened using RNA sequencing (RNA‑seq) and validated by co‑immunoprecipitation and co‑immunofluorescence. The underlying signaling pathway was investigated by western blotting and functional rescue experiments. The results demonstrated that knockdown of ITGB4 significantly suppressed CRC cell proliferation, migration and invasion, while promoting apoptosis <i>in vitro</i>. Similarly, silencing ITGB4 markedly inhibited tumor growth in the <i>in vivo</i> xenograft model. RNA‑seq analysis identified Ezrin (EZR) as a key downstream target of ITGB4, and a direct protein‑protein interaction was confirmed between them. Mechanistically, ITGB4 knockdown decreased the expression of EZR at both the mRNA and protein levels. ITGB4 was demonstrated to exert its pro‑tumorigenic effects through the regulation of EZR, which subsequently activated the Wnt/β‑catenin signaling pathway. Interestingly, EZR overexpression partially restored ITGB4 levels, suggesting a hypothetical positive feedback loop via Wnt/β‑catenin signaling that could amplify this oncogenic axis. Notably, the malignant phenotypes suppressed by ITGB4 silencing were significantly rescued by the overexpression of EZR. In conclusion, the present study identified a novel ITGB4/EZR/Wnt/β‑catenin signaling axis in CRC. ITGB4 promotes CRC progression by modulating EZR expression and subsequently activating the Wnt/β‑catenin pathway. These findings highlight ITGB4 as a potential prognostic biomarker and a promising therapeutic target for CRC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147987489","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}