International Journal Of Oncology[JOURNAL]
Sun
200 papers
Emerging insights into alternative end‑joining: Mechanisms, genome instability and therapeutic opportunities in cancer (Review).
Azam N, Liu X, Li X … +2 more , Ma L, Liu Q
Int J Oncol · 2025 Dec · PMID 41070620 · Full text
Genome instability is a central hallmark of cancer, driven by aberrant DNA damage responses that facilitate tumor evolution and resistance to therapy. Although canonical non‑homologous end joining and homologous recombin...
Genome instability is a central hallmark of cancer, driven by aberrant DNA damage responses that facilitate tumor evolution and resistance to therapy. Although canonical non‑homologous end joining and homologous recombination are well‑characterized pathways for repairing DNA double‑strand breaks (DSBs), recent advances have revealed that cancer cells increasingly depend on alternative end‑joining (alt‑EJ) to survive persistent DNA damage that arises from intrinsic stresses or external therapies. Alt‑EJ, characterized by its reliance on microhomologous sequences at DSB sites, promotes mutation accumulation and chromosomal rearrangements, thereby driving genomic instability and tumor progression. Despite its pivotal role in cancer biology, the molecular regulation, contextual determinants and dualistic role of alt‑EJ in maintaining genome integrity compared with promoting instability remain incompletely understood. The present review integrated the latest mechanistic insights into alt‑EJ, elucidated its regulatory networks and interactions with canonical DSB repair pathways and discussed its consequences for cancer genome integrity and evolution. Furthermore, it highlighted the emerging potential of alt‑EJ as a therapeutic vulnerability for cancer, underscoring the urgent need to translate these discoveries into innovative treatment strategies aimed at overcoming therapy resistance and improving patient outcomes.
Exosomal microRNAs: A new role in the diagnosis and treatment of lung cancer metastases (Review).
Li X, Wang J, Ge W … +1 more , Chen X
Int J Oncol · 2025 Dec · PMID 41070615 · Full text
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 pr...
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.
Adipocyte‑derived extracellular vesicles sustain mitochondrial metabolism in breast cancer cells: New insights into the cross‑talk between cancer cells and the tumor microenvironment.
Gelsomino L, Del Console P, Murfuni MS … +12 more , Gaspari M, Giordano F, Naimo GD, Fiorillo M, Arpino G, Giuliano M, Panza S, Bonofiglio D, Andò S, Barone I, Giordano C, Catalano S
Int J Oncol · 2025 Dec · PMID 41070614 · Full text
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 tha...
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.
Application of cfDNA methylation in cancer prognostic assessment: Progress and challenges (Review).
Su C, Wu J, Jiang L … +6 more , Lv T, Liu W, Zhang J, Zhang Y, Peng X, Tan J
Int J Oncol · 2025 Dec · PMID 40999985 · Full text
Cancer prognostic assessment constitutes an essential component of cancer treatment and management. It encompasses the prediction of patients' disease progression, treatment effect and survival. Circulating free DNA (cfD...
Cancer prognostic assessment constitutes an essential component of cancer treatment and management. It encompasses the prediction of patients' disease progression, treatment effect and survival. Circulating free DNA (cfDNA) refers to highly fragmented DNA that exists extracellularly in the human bloodstream. Its methylation status is not only a reliable indicator for the prognosis of cancer, but also a highly accurate predictor of the prognosis of cancer. As an emerging non‑invasive biomarker, cfDNA has demonstrated considerable potential in cancer prognostic assessment in recent years. The present review provided a comprehensive review of the promising applications of cfDNA methylation in cancer prognostic assessment, while also discussing the challenges that must be addressed to fully realize its clinical potential. As technology advances and research deepens, cfDNA methylation is expected to play an increasingly pivotal role in the field of cancer precision medicine.
[Expression of Concern] Podoplanin‑mediated TGF‑β‑induced epithelial-mesen-chymal transition and its correlation with bHLH transcription factor DEC in TE‑11 cells.
Wu Y, Liu Q, Yan X … +6 more , Kato Y, Tanaka M, Inokuchi S, Yoshizawa T, Morohashi S, Kijima H
Int J Oncol · 2025 Dec · PMID 40999984 · Full text
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 'podoplani...
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].
ZBTB20 promotes ferroptosis through inhibiting TMEM109 expression in glioblastoma cells.
Chen X, Luo M, Niu X … +5 more , Wang W, Cao H, Zhang L, Wei R, Duan P
Int J Oncol · 2025 Dec · PMID 40999982 · Full text
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 (), a transcription repressor, is expr...
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 (), a transcription repressor, is expressed at low levels in GBM and suppresses GBM cell proliferation through the ERK signaling pathway. However, the effect of 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 expression and ferroptosis levels in GBM cells were lower than that in normal glial cells. Gain‑ and loss‑of‑function experiments revealed that overexpression promoted ferroptosis and knockdown inhibited ferroptosis in GBM cells. Moreover, the results demonstrated that transcriptionally repressed the expression of transmembrane protein 109 () 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 overexpression inhibited ferroptosis and knockdown promoted ferroptosis in GBM cells. Using co‑transfection experiments, it was further revealed that the promotive effect of can reverse the inhibitory effect of TMEM109 on ferroptosis. In conclusion, the findings indicated that promotes ferroptosis in GBM cells through transcriptionally repressing the expression of .
[Expression of Concern] miR‑135b, upregulated in breast cancer, promotes cell growth and disrupts the cell cycle by regulating LATS2.
Hua K, Jin J, Zhao J … +8 more , Song J, Song H, Li D, Maskey N, Zhao B, Wu C, Xu H, Fang L
Int J Oncol · 2025 Dec · PMID 40970336 · Full text
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 st...
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].
Cooperation between ZEB2 and SP1 upregulates PD‑L1 and CCL2 to promote the immunosuppressive activity of tumor cells.
Ko D, Lee Y, Yoon J … +3 more , Choi EK, Jang D, Kim S
Int J Oncol · 2025 Nov · PMID 40970322 · Full text
Epithelial‑mesenchymal transition (EMT) is implicated in tumor progression and EMT‑inducing transcription factors play multifaceted roles; however, the molecular mechanisms underlying these processes are not well underst...
Epithelial‑mesenchymal transition (EMT) is implicated in tumor progression and EMT‑inducing transcription factors play multifaceted roles; however, the molecular mechanisms underlying these processes are not well understood. Previously, we showed that ZEB2 acts cooperatively with the transcription factor SP1 to function as a transcriptional activator that promotes cancer cell invasion and survival, as well as angiogenesis. The present study reported a novel role for Zinc Finger E‑Box Binding Homeobox 2 (ZEB2) in conferring immunosuppressive activity on cancer cells, as well as the underlying molecular mechanism. ZEB2 cooperated with SP1 to upregulate transcription of and by interacting with the proximal SP1 element in their promoters. ZEB2‑mediated programmed cell death 1 ligand 1 (PD‑L1) upregulation on tumor cells inhibited T cell activation and cytokine secretion in a co‑culture system. ZEB2 upregulated C‑C motif chemokine ligand 2 (CCL2) secretion to promote migration of macrophages and drive polarization to an M2‑like phenotype. ZEB2 suppressed the activity of tumor‑infiltrating T cells in a syngeneic mouse tumor model. Furthermore, SUMOylation of ZEB2 by PC2 was required for efficient cooperation between ZEB2 and SP1, as well as for subsequent gene expression. Clinical data showed that expression is associated positively with expression of and . Expression of both and or has prognostic significance for predicting survival of colon cancer patients. The present study demonstrated a previously unrecognized role for ZEB2: Direct modulation of the interaction between tumor cells and immune cells. Taken together, the data increased our understanding of the molecular mechanism underlying immunosuppression mediated by an EMT‑inducing transcription factor.
[Corrigendum] Lithium chloride induces mesenchymal‑to‑epithelial reverting transition in primary colon cancer cell cultures.
Costabile V, Duraturo F, Delrio P … +8 more , Rega D, Pace U, Liccardo R, Rossi GB, Genesio R, Nitsch L, Izzo P, De Rosa M
Int J Oncol · 2025 Nov · PMID 40937581 · Full text
Following the publication of the above article, an interested reader drew the authors' attention to the fact that the CTK18 panel in Fig. 2E on p. 1917, showing the results of RT‑PCR analysis of cytokeratin 18 from patie...
Following the publication of the above article, an interested reader drew the authors' attention to the fact that the CTK18 panel in Fig. 2E on p. 1917, showing the results of RT‑PCR analysis of cytokeratin 18 from patient no. 88, appeared to be very similar to the CTK18 panel in Fig. 2F (showing the results from patient no. 93). After having re‑examined their original data, which were also presented to the Editorial Office, and considering that the observed experiment is an end-point RT-PCR performed more than ten years ago, the authors cannot definitively rule out the possibility that Fig. 2E was inadvertently misassembled. Therefore, given the high similarity of the two images, it was decided to publish a revised version of Fig. 2, which now shows data from a different replicate of the experiment for the CTK18 panel in Fig. 2E, shown on the next page. Note that this revision did not affect the overall conclusions reported in the study. The authors are grateful to the Editor of 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 46: 1913‑1923, 2015; DOI: 10.3892/ijo.2015.2911].
Progerin regulates actin cytoskeletal remodeling and inhibits EMT and metastasis in triple‑negative breast cancer cells.
Huang X, Luo W, Liu W … +2 more , Liu X, Chen W
Int J Oncol · 2025 Nov · PMID 40937572 · Full text
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 transit...
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.
Potential of Fibulin2 as a therapeutic target against cancer and as a diagnostic marker (Review).
Yang Y, Wang Z, Weng L … +2 more , Fei J, Li Z
Int J Oncol · 2025 Nov · PMID 40937555 · Full text
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 compo...
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.
[Corrigendum] Furin promotes epithelial‑mesenchymal transition in pancreatic cancer cells via Hippo‑YAP pathway.
Zhang Y, Zhou M, Wei H … +10 more , Zhou H, He J, Lu Y, Wang D, Chen B, Zeng J, Peng W, Du F, Gong A, Xu M
Int J Oncol · 2025 Nov · PMID 40878952 · Full text
Following the publication of the above article, the authors drew to the Editor's attention that the image in Fig. 3A on p. 1356 for the 'Migration/BxPC3/sh‑EGFP' experiment was mistakenly presented. This error arose as a...
Following the publication of the above article, the authors drew to the Editor's attention that the image in Fig. 3A on p. 1356 for the 'Migration/BxPC3/sh‑EGFP' experiment was mistakenly presented. This error arose as a consequence of a mistake that was made during the preparation of the final images. Furthermore, upon performing an independent analysis of the data in this paper in the Editorial Office, it came to light that, for the colony‑formation assay experiments shown in Fig. 2F on p. 1355, the image selected for the 'PaTu8988/Flag‑Furin' experiment had already appeared in a different context in another paper published by the same authors, also in the journal . After having examined their original data, the authors realize that this second figure in the paper had also been inadvertently assembled incorrectly. The revised versions of Fig. 2 (now showing the data correctly for the for the 'PaTu8988/Flag‑Furin' experiment) and Fig. 3 (showing the correct data for the 'Migration/BxPC3/sh‑EGFP' experiment) are shown on the next two pages. Note that the errors made during the compilation of these figures did not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 50: 1352‑1362, 2017; DOI: 10.3892/ijo.2017.3896].
[Expression of Concern] 4‑Hydroxybutenolide impairs cell migration, and invasion of human oral cancer SCC‑4 cells via the inhibition of NF‑κB and MAPK signaling pathways.
Yu FS, Lin ML, Hsu SC … +4 more , Yu CC, Huang YP, Kuo YH, Chung JG
Int J Oncol · 2025 Nov · PMID 40878940 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell assay data shown in Fig. 2C on p. 582, the '24 h/1 M' and '24 h/2.5 M' data panels contai...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell assay data shown in Fig. 2C on p. 582, the '24 h/1 M' and '24 h/2.5 M' data panels contained an overlapping section of cellular data; in addition, the '24 h/Control' and '48 h/Control' panels in Fig. 2E similarly contained an overlapping section of data, such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original sources. Upon analyzing the data independently in the Editorial Office, it came to light that the '0 h/1 M' and '12 h/2.5 M' data panels in Fig. 2A (showing the results of scratch‑wound assay experiments) also contained an overlapping area, albeit the 12 h/2.5 M' data panel had been rotated through 180° relative to the '0 h/1 M' panel. 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, 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 49: 579‑588, 2016; DOI: 10.3892/ijo.2016.3537].
Role of metabolic reprogramming of cancer‑associated fibroblasts in tumor development and progression (Review).
Li R, Li Y
Int J Oncol · 2025 Nov · PMID 40878935 · Full text
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, ca...
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.
Functional mechanisms of circular RNA‑encoded peptides and future research strategies and directions in nasopharyngeal carcinoma (Review).
Xu W, Ma Z, Gong W … +2 more , Fu S, Chen X
Int J Oncol · 2025 Oct · PMID 40849819 · Full text
Nasopharyngeal carcinoma (NPC) is an epithelial malignancy closely associated with Epstein‑Barr virus (EBV) infection. Although patients with early‑stage NPC can achieve a high cure rate through radiotherapy, recurrence...
Nasopharyngeal carcinoma (NPC) is an epithelial malignancy closely associated with Epstein‑Barr virus (EBV) infection. Although patients with early‑stage NPC can achieve a high cure rate through radiotherapy, recurrence and distant metastasis remain the primary causes of treatment failure in patients with advanced‑stage NPC. Circular RNA (circRNA) is a class of covalently closed non‑coding RNAs involved in multiple aspects of tumor biology. Recent evidence has shown that certain circRNAs can encode functional peptides, which participate in the regulation of tumor‑related signaling pathways. In NPC, circRNAs have been implicated in the modulation of signaling pathways, including NF‑κB and JAK/STAT, both of which are activated in the EBV‑infected microenvironment. Furthermore, frequently mutated genes in NPC, such as TNF receptor‑associated factor 3 and cylindromatosis lysine 63 deubiquitinase, are known regulators of the NF‑κB pathway, suggesting a potential link between genetic alterations and circRNA‑related mechanisms. This article systematically reviews the biological mechanisms of circRNA‑encoded peptides, summarizes the expression and function of circRNA in NPC and focuses on discussing the potential roles of circRNA‑encoded peptides in tumor microenvironment regulation, immune escape and clinical application prospects. By integrating existing research results, this article aims to provide a new perspective and theoretical basis for the in‑depth exploration of circRNA‑encoded peptides in the field of NPC.
[Corrigendum] Identification of Akt1 as a potent therapeutic target for oral squamous cell carcinoma.
Nakashiro KI, Tanaka H, Goda H … +6 more , Iwamoto K, Tokuzen N, Hara S, Onodera J, Hino S, Hamakawa H
Int J Oncol · 2025 Oct · PMID 40849817 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the western blots shown in Figs. 1C and 3A, the six lanes for the control β‑tubulin blots shown i...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the western blots shown in Figs. 1C and 3A, the six lanes for the control β‑tubulin blots shown in Fig. 1C appeared strikingly similar to the β‑tubulin blots in Fig. 3A, albeit the bands in Fig. 3A appeared to have been horizontally stretched. The authors were able to check their original data, and realized that Fig. 3 had inadvertently been assembled incorrectly. A revised version of Fig. 3, now showing data for both the Akt1 and β‑tubulin blots from one of the repeated experiments, is shown opposite. All authors confirm that the errors made in assembling Fig. 3 did not have a major impact on the conclusions reported in the above article, and they thank the Editor of for allowing them the opportunity to publish a Corrigendum. Furthermore, all the authors agree to the publication of this Corrigendum, and apologize to the readers for any inconvenience caused. [International Journal of Oncology 47: 1273‑1281, 2015; DOI: 10.3892/ijo.2015.3134].
Unraveling tumor cell‑tumor microenvironment crosstalk through antibody array technologies (Review).
Wang Y, Luo S, Dong H … +1 more , Huang RP
Int J Oncol · 2025 Oct · PMID 40849816 · Full text
The tumor microenvironment (TME) consists of tumor cells, stromal cells, infiltrating immune cells and non‑cellular components such as extracellular matrix, blood vessels and a wide variety of secreted proteins. Evidence...
The tumor microenvironment (TME) consists of tumor cells, stromal cells, infiltrating immune cells and non‑cellular components such as extracellular matrix, blood vessels and a wide variety of secreted proteins. Evidence shows that beyond supporting tumor growth, the TME also promotes tumor cell proliferation and invasion and contributes to treatment resistance, ultimately affecting patient prognosis. Cell‑to‑cell communication within the TME is driven by secreted proteins such as cytokines, chemokines, growth factors and interferons, which are produced not only by tumor cells but also by various stromal cells and immune cells. These proteins form a complex signaling network that promotes tumor cell proliferation and invasion and enables tumors to evade innate and adaptive immune responses. Antibody arrays are a technology that can simultaneously screen hundreds of secreted proteins in complex biological samples, aiding in the exploration of this complex signaling network. By combining high‑throughput multiplex immunoassays such as antibody arrays with cellular and molecular biology techniques, researchers have uncovered complex regulatory mechanisms of cytokine networks within the TME. The present review summarized recent findings on the communication between tumor cells and the TME, as well as key secreted proteins essential for tumor progression and the development of therapeutic resistance. In addition, it discusses how high‑throughput antibody arrays contribute to our understanding of regulatory networks of secreted proteins in the TME.
Nanoparticle‑based delivery systems for targeted therapy in brain tumors: Progress, challenges and perspectives (Review).
Si JX, Liu ZC, Gu F … +2 more , Jin X, Ma YY
Int J Oncol · 2025 Oct · PMID 40849813 · Full text
Brain tumors, particularly gliomas, are among the most lethal malignancies, with high mortality driven by a delayed diagnosis and limited therapeutic efficacy. A central challenge lies in the presence of the blood‑brain...
Brain tumors, particularly gliomas, are among the most lethal malignancies, with high mortality driven by a delayed diagnosis and limited therapeutic efficacy. A central challenge lies in the presence of the blood‑brain barrier (BBB), which severely impedes the delivery of systemically administered therapeutics to tumor sites. Addressing this clinical urgency, nanoparticle (NP)‑based delivery systems have emerged as a transformative strategy to enhance brain‑specific drug accumulation, minimize off‑target toxicity and improve treatment outcomes. The present review systematically examined the recent advances in nanocarrier technologies for targeted brain tumor therapy, including liposomes, solid lipid NPs, dendrimers, polymeric nanoplatforms and inorganic nanomaterials. The design principles, mechanisms for BBB traversal, therapeutic payload compatibility and tumor‑targeting capabilities of NP technologies demonstrated in preclinical models have also been highlighted. In addition to drug delivery, emerging applications of nanocarriers in gene therapy were explored and the impact of protein corona formation on NP behavior was discussed. Finally, current translational bottlenecks were identified and future design considerations to achieve clinically viable, precision‑targeted nanomedicines for brain tumors were outlined.
Notch3 mediated TGF‑β1 activation enhances epithelial‑mesenchymal transition and cancer stemness in non‑small lung cancer.
Wang F, Hu S, Bian J … +5 more , Gao Q, Cao L, Sang L, Yang J, Xu X
Int J Oncol · 2025 Oct · PMID 40849808 · Full text
Notch3 is a key regulator in various cancers, playing a crucial role in maintaining stemness and promoting epithelial‑mesenchymal transition (EMT). However, its differential expression and regulatory mechanisms in non‑sm...
Notch3 is a key regulator in various cancers, playing a crucial role in maintaining stemness and promoting epithelial‑mesenchymal transition (EMT). However, its differential expression and regulatory mechanisms in non‑small cell lung cancer (NSCLC) and cancer stem cells remain poorly understood. To investigate this, the present study examined Notch3 expression in NSCLC through Oncomine, The Cancer Genome Atlas and Gene Expression Omnibus databases and validated the results with immunohistochemistry, reverse transcription‑quantitative PCR and western blotting. EMT was induced by TGF‑β1 in NSCLC cells and functional assays (Transwell, wound healing and sphere formation) were performed to assess cellular changes. experiments using a xenograft mouse model were conducted to evaluate tumor growth and metastasis. The results showed that high Notch3 expression was associated with poor prognosis in NSCLC patients. Downregulation of Notch3 inhibited TGF‑β1‑induced EMT and CSC characteristics, resulting in reduced tumorigenic potential, whereas overexpression of the Notch3 intracellular domain enhanced these effects. Silencing Notch3 suppressed EMT and markedly inhibited tumor growth and metastasis . These findings demonstrated that Notch3 regulated EMT and CSC properties in NSCLC, promoting tumor recurrence and metastasis. Notch3 thus represents a promising therapeutic target and prognostic marker for NSCLC.
Harnessing TP73‑targeted nintedanib: A novel strategy to halt triple‑negative breast cancer via p53‑PPARα/PI3K‑Akt pathway suppression.
Zou X, Li S, Huang S … +3 more , Niu R, Liu G, Wang Z
Int J Oncol · 2025 Nov · PMID 40849803 · Full text
Triple‑negative breast cancer (TNBC) is an aggressive malignancy with limited treatment options, leading to poor clinical outcomes and the need for novel therapeutic approaches. Nintedanib, a United States Food and Drug...
Triple‑negative breast cancer (TNBC) is an aggressive malignancy with limited treatment options, leading to poor clinical outcomes and the need for novel therapeutic approaches. Nintedanib, a United States Food and Drug Administration‑approved multi‑kinase inhibitor with anti‑fibrotic and anti‑angiogenic properties, has shown promise in cancer treatment. However, its precise molecular effects on TNBC have not yet been fully elucidated. Therefore, the present study aimed to investigate the therapeutic potential of nintedanib in TNBC using and models, specifically focusing on its regulatory effects on key oncogenic pathways. The present study utilized TNBC cell lines (MDA‑MB‑231 and 4T1) and BALB/c mice to evaluate the antitumor efficacy of nintedanib. Cell viability and clonogenic capacity were assessed using Cell Counting Kit‑8 and colony formation assays. Subsequently, apoptosis induction and cell cycle progression were determined by flow cytometry, and cell migration and invasion were analyzed through scratch and Transwell assays. To identify underlying mechanisms, potential molecular targets were identified via bioinformatics and network pharmacology, and were validated through western blotting, immunofluorescence and immunohistochemistry. Finally, an orthotopic TNBC mouse model was established and monitored in real time by multimodal ultrasound imaging. The results revealed that nintedanib significantly inhibited TNBC cell proliferation and suppressed stem cell‑like properties. Furthermore, it induced cell cycle arrest at the G/M phase and promoted apoptosis. Mechanistic analysis revealed that nintedanib activated tumor protein p73 (TP73), leading to the disruption of the p53‑peroxisome proliferator‑activated receptor α (PPARα)/PI3K‑Akt signaling axis. Additionally, it downregulated epithelial‑mesenchymal transition (EMT) markers, including Snail and zinc finger E‑box‑binding homeobox protein 1, thereby mitigating tumor invasiveness. , nintedanib treatment effectively reduced tumor growth, angiogenesis and stiffness, indicating its potential as a viable therapeutic agent for TNBC. In conclusion, nintedanib exerts potent anti‑TNBC effects by modulating TP73, disrupting oncogenic signaling via the p53‑PPARα/PI3K‑Akt axis, and attenuating EMT‑associated transcription factors. These findings highlight its potential as a promising targeted therapy for TNBC, warranting further clinical exploration.
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