International Journal Of Oncology[JOURNAL]
Sun
200 papers
Circulating proteins as biomarkers of response to cancer immunotherapy (Review).
Pinard C, Ginzac A, Abrial C … +2 more , Durando X, Radosevic-Robin N
Int J Oncol · 2026 Jul · PMID 42099246 · Full text
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 biomar...
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.
[Corrigendum] Tumor necrosis factor‑α triggers opposing signals in head and neck squamous cell carcinoma and induces apoptosis via mitochondrial‑ and non‑mitochondrial‑dependent pathways.
Selimovic D, Wahl RU, Ruiz E … +9 more , Aslam R, Flanagan TW, Hassan SY, Santourlidis S, Haikel Y, Friedlander P, Megahed M, Kandil E, Hassan M
Int J Oncol · 2026 Jul · PMID 42059273 · Full text
Following the publication of the above article, an interested reader drew to the Editor's attention that a number of western blots in the paper appeared to contain incorrectly assembled data. First, comparing the F. Leng...
Following the publication of the above article, an interested reader drew to the Editor's attention that a number of western blots in the paper appeared to contain incorrectly assembled data. First, comparing the F. Length (full‑length) Caspase 3 blots in Fig. 1F with the p‑ASK1 blots in Fig. 2C revealed that they were remarkably similar after horizontally flipping one set of the bands. In addition, the cytochrome c (Cyt. C) bands in Fig. 1F were similarly found to be remarkably similar to the IκBα blots in Fig. 2A, again after horizontal flipping of one set of the bands. Finally, it was noted that the β‑actin bands in Fig. 5C were very similar to the blots included in Fig. 3B to show the Tom20 data. After having examined the raw data underling these figures (which were also presented to the Editorial Office for our inspection), the authors realized that data in Figs. 1, 2, 3 and 5 were inadvertently assembled incorrectly in these figures. The revised versions of Figs. 1, 2, 3 and 5 are shown on the subsequent six pages. Specifically, in Fig. 1F, the blot for Cyt. C was incorrectly chosen; in Fig. 2A, the blot for IkBα was incorrectly chosen; in Fig. 3B, the blot for Tom20 was incorrectly chosen; and in Fig. 5C, the β‑actin blots shown to represent the gels for both the treated and control CLS‑354 and RPMI 2650 cells were incorrectly placed in this figure. These data have all been replaced with the correct data in the figures shown subsequently in this Corrigendum. The authors regret that the errors in Figs. 1F, 2A, 2C, 3B and 5C went unnoticed in the published versions of these figures in this paper, although note that these errors did not influence either the validity of the published data or the conclusions described in the article. The authors are grateful to the Editor of for allowing them the opportunity to publish this Corrigendum. All the authors agree with the publication of this Corrigendum, and apologize to the readership for any inconvenience caused. [International Journal of Oncology 55: 1324‑1338, 2019; DOI: 10.3892/ijo.2019.4900].
Research advances in aptamers in the diagnosis and treatment of breast cancer (Review).
Chu L, Xiao Y, Li X … +4 more , Cui J, Ma L, Shao B, Cui H
Int J Oncol · 2026 Jun · PMID 42028740 · Full text
Cancer is a malignant disease that threatens human life and health. Among cancer types, breast cancer is one of the most common malignant tumors in women worldwide and ranks among the top cancer types in terms of inciden...
Cancer is a malignant disease that threatens human life and health. Among cancer types, breast cancer is one of the most common malignant tumors in women worldwide and ranks among the top cancer types in terms of incidence rate of malignant tumors in Chinese women. Aptamers are a class of DNA or RNA sequences that can bind to specific targets through their three‑dimensional structures, and are screened and obtained via systematic evolution of ligands by exponential enrichment technology. Aptamers have advantages of high affinity and specificity, strong stability, low immunogenicity, a wide range of targets and ease of preparation and purification. As effective molecular targeting tools and drug delivery carriers, aptamers and their conjugates show therapeutic potential in the early diagnosis and treatment of breast cancer. The present article reviewed the properties and screening techniques of aptamers, as well as their applications and research progress in the diagnosis and treatment of breast cancer, with the aim of providing new strategies and directions for the realization of precision medicine for breast cancer via aptamers.
[Retracted] MicroRNA‑155 promotes tumor growth of human hepatocellular carcinoma by targeting ARID2.
Zhang L, Wang W, Li X … +5 more , He S, Yao J, Wang X, Zhang D, Sun X
Int J Oncol · 2026 Jun · PMID 42028735 · Full text
Following the publication of the above paper, a concerned reader drew to the Editor's attention that, in addition to concerns about the description of one of the antibodies employed in this study, the immunohistochemical...
Following the publication of the above paper, a concerned reader drew to the Editor's attention that, in addition to concerns about the description of one of the antibodies employed in this study, the immunohistochemical data shown in Fig. 4E on p. 2429 and western blot data shown in Fig. 6E on p. 2431 had apparently appeared in figures in other papers that had already been submitted to the journals Oncotarget and respectively, both of which were written by different authors at different research institutes. Upon performing an independent analysis of the data in the Editorial Office, we were able to validate these concerns; moreover, some of the same western blot data had also apparently been included in Figs. 4 and 5. Given that the abovementioned data had already been submitted for publication to other journals, the Editor of has decided that this article should be retracted from the Journal. 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 48: 2425‑2434, 2016; DOI: 10.3892/ijo.2016.3465].
METTL3 in esophageal cancer: Current insights into molecular mechanisms, subtype heterogeneity and targeted therapy prospects (Review).
Pu C, Hu H, Fan H … +2 more , Chen T, Tang J
Int J Oncol · 2026 Jun · PMID 42028733 · Full text
Esophageal cancer (EC), comprising esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), urgently requires novel targeted therapies. The mA methyltransferase METTL3 has emerged as a critical epit...
Esophageal cancer (EC), comprising esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), urgently requires novel targeted therapies. The mA methyltransferase METTL3 has emerged as a critical epitranscriptomic regulator in gastrointestinal malignancies. In ESCC, METTL3 functions predominantly as an oncogene, driving tumor progression via mA‑dependent modulation of RNA stability, splicing, and translation across key networks, including NOTCH1, EGR1/Snail and Wnt/β‑catenin. Conversely, hypotheses regarding mA‑independent functions or direct immune‑checkpoint regulation remain unvalidated in EC. Crucially, METTL3 actively modulates DNA damage repair and radiotherapy resistance, exposing a promising therapeutic vulnerability, although clinical pharmacological development remains nascent. Furthermore, METTL3 biology in EAC remains conspicuously uncharacterized. By strictly stratifying evidence by EC subtype, the present review distinguishes empirically validated mechanisms from premature cross‑cancer extrapolations. Ultimately, a novel conceptual framework that redefines METTL3 not merely as a static oncogene, but as a dynamic, context‑dependent regulatory hub, is proposed. Under therapeutic stress, METTL3 amplifies cellular phenotypic plasticity, systematically orchestrating tumor adaptation and treatment resistance.
Biomarkers for oesophageal squamous cell carcinoma and the role of HPV: Multi‑omics approaches and current evidence (Review).
Zou L, Zhao H, Zhang J … +7 more , Xie J, An X, Qi X, Yue Y, Zhang L, Zhang X, Liu K
Int J Oncol · 2026 Jun · PMID 42028731 · Full text
Oesophageal squamous cell carcinoma (ESCC) represents a major global health burden, particularly in regions with high incidence rates, significantly affecting patient quality of life and survival outcomes. Recent advance...
Oesophageal squamous cell carcinoma (ESCC) represents a major global health burden, particularly in regions with high incidence rates, significantly affecting patient quality of life and survival outcomes. Recent advances in multi‑omics technologies have highlighted their potential in identifying prognostic markers for ESCC. Concurrently, the possible association between human papillomavirus (HPV) infection and ESCC development has been investigated, although epidemiological evidence remains heterogeneous and a definitive causal role has not been universally established. This narrative review examines the progress in multi‑omics approaches for identifying prognostic markers of ESCC and provides a comprehensive analysis of the latest developments in HPV detection methods. Research from genomic, transcriptomic, proteomic, epigenomic, metabolomic, and immunomic studies was synthesized highlighting both promising biomarkers and the significant heterogeneity in reported results, particularly regarding HPV prevalence rates across various geographical regions and detection methods. The research included not only offers novel insights into the pathogenesis of ESCC but also lays a theoretical foundation for early diagnosis and personalized treatment; however, most findings remain investigational and require prospective validation before clinical implementation. The clinical implications and future research directions are discussed with consideration of current limitations.
[Expression of Concern] AHIF promotes glioblastoma progression and radioresistance via exosomes.
Dai X, Liao K, Zhuang Z … +11 more , Chen B, Zhou Z, Zhou S, Lin G, Zhang F, Lin Y, Miao Y, Li Z, Huang R, Qiu Y, Lin R
Int J Oncol · 2026 Jun · PMID 41992982 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 2E on p. 264, the Transwell invasion assay results shown in the "T98G‑AHIF KD" data panel appeared...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 2E on p. 264, the Transwell invasion assay results shown in the "T98G‑AHIF KD" data panel appeared to potentially contain an overlapping section with the "U251‑AHIF OE" data panel in Fig. 3E. 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; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 54: 261‑270, 2019; DOI: 10.3892/ijo.2018.4621].
Novel therapeutic strategies for metastatic castration‑resistant prostate cancer: Beyond androgen receptor pathway inhibition (Review).
Wang Y, Xie Y, Zhao Q
Int J Oncol · 2026 Jun · PMID 41992975 · Full text
Metastatic castration‑resistant prostate cancer (mCRPC) remains a lethal disease due to universal resistance to androgen‑receptor pathway inhibitors (ARPI). Tumor progression is orchestrated by a spectrum of androgen‑rec...
Metastatic castration‑resistant prostate cancer (mCRPC) remains a lethal disease due to universal resistance to androgen‑receptor pathway inhibitors (ARPI). Tumor progression is orchestrated by a spectrum of androgen‑receptor‑independent drivers, including genomic alterations in DNA damage repair pathways, epigenetic shifts promoting lineage plasticity, metabolic adaptations and an immunosuppressive tumor microenvironment. This evolving understanding has catalyzed the development of novel therapeutic strategies. These include PARP inhibitors for tumors with homologous recombination repair deficiencies, protein kinase B inhibitors for the phosphatase and tensin homolog‑loss subset, prostate‑specific membrane antigen (PSMA)‑targeted radioligand therapy, bispecific T‑cell engagers, antibody‑drug conjugates and immune checkpoint inhibitors. Furthermore, liquid biopsy profiling, PSMA‑positron emission tomography‑based radiomics and artificial intelligence platforms are enhancing real‑time patient selection and response assessment. The present review synthesized these recent preclinical and clinical advances to delineate biomarker‑driven, mechanism‑based therapeutic sequencing and combination strategies for mCRPC in the post‑ARPI era.19.
RRP9 suppresses hepatocellular carcinoma progression by inhibiting the PI3K/AKT/mTOR pathway.
Fu Z, Li M, Dong K … +2 more , Feng J, Wang W
Int J Oncol · 2026 Jun · PMID 41952494 · Full text
Ribosomal RNA processing 9 (RRP9) encodes a WD‑repeat domain‑containing protein, which is a potential carcinogenic biomarker for various tumors. As a key structural component of small nucleolar ribonucleoproteins, RRP9 s...
Ribosomal RNA processing 9 (RRP9) encodes a WD‑repeat domain‑containing protein, which is a potential carcinogenic biomarker for various tumors. As a key structural component of small nucleolar ribonucleoproteins, RRP9 serves a key role in ribosome biogenesis by facilitating 18S rRNA processing. Despite its association with the pathogenesis of various malignancies, its function and molecular mechanisms in hepatocellular carcinoma (HCC) remain unknown. The present study aimed to examine the biological role of RRP9 in HCC progression and the underlying regulatory mechanisms. Immunohistochemical and western blot analyses revealed a significant downregulation of RRP9 expression in patients with HCC compared with matched adjacent non‑tumorous tissues. To investigate RRP9 biological functions in HCC, stable RRP9‑knockdown and ‑overexpressing isogenic HCC cell line models were established using lentiviral transduction and puromycin selection. Functional assays, including Cell Counting Kit‑8 viability, colony formation, wound healing migration and Transwell invasion experiments, consistently demonstrated that RRP9 significantly suppressed HCC cell viability, proliferation, invasion and migration. Transcriptome sequencing and western blot analyses indicated that RRP9 inhibited the PI3K/AKT/mTOR pathway. Furthermore, functional rescue assays using the PI3K activator 740 Y‑P and the inhibitor PI3K/AKT/mTOR‑IN‑2 verified that RRP9 exerts its tumor‑suppressive role via this pathway. Protein‑protein interaction analysis revealed an association between RRP9 and cyclin A2 (CCNA2). Western blotting confirmed that RRP9 downregulated CCNA2 expression. Additionally, subcutaneous tumorigenesis in mice showed that RRP9 inhibits liver cancer progression via the PI3K/AKT/mTOR signaling pathway.
[Corrigendum] PRIMA‑1 inhibits growth of breast cancer cells by re‑activating mutant p53 protein.
Liang Y, Besch-Williford C, Hyder SM
Int J Oncol · 2026 Jun · PMID 41952491 · Full text
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, regarding the immunohistochemical images shown in Fig. 1B on p. 1018, the 'PAb1620/PM 25μM' and 'PAb1620/PM...
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, regarding the immunohistochemical images shown in Fig. 1B on p. 1018, the 'PAb1620/PM 25μM' and 'PAb1620/PM 50μM' data panels shown in Fig. 1B for the T47‑D and HCC‑1428 cell lines were apparently the same, sugggesting that this figure had been assembled incorrectly. After re‑examining their original data, the authors have realized that the 'PAb1620/PM 25μM' and 'PAb1620/PM 50μM' data panels correctly shown for the T47‑D cell line had inadvertently been copied across for the HCC‑1428 cell line. The revised version of Fig. 1, now showing all the correct data for the HCC‑1428 cell line in Fig. 1B, is shown below. The authors are grateful to the Editor of for allowing them this opportunity to publish a Corrigendum, and all the authors agree to its publication. Note that this error did not grossly affect either the results or the conclusions reported in this study; furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 35: 1015‑1023, 2009; DOI: 10.3892/ijo_00000416].
[Retracted] Antitumor activity of NRC‑AN‑019 in a pre‑clinical breast cancer model.
Gondi CS, Gorantla B, Rao AKSB … +7 more , Amala K, Naidu MUR, Jogi KV, Ramana GV, Myneni PC, Junnarkar A, Rao JS
Int J Oncol · 2026 Jun · PMID 41930470 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the 'Control' tumor images shown in Fig. 6A on p. 647 were unexpectedly similar to the tumor imag...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the 'Control' tumor images shown in Fig. 6A on p. 647 were unexpectedly similar to the tumor images shown five rows down for the 30 mg/kg Lapatinib administration experiment, albeit the images were turned through 180°. Owing to the fact that this figure appeared to have been assembled erroneously, and that data may have been duplicated within the figure to show the results of apparently different experiments, the Editor of has decided that this paper should be retracted from the Journal. 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 39: 641‑648, 2011; DOI: 10.3892/ijo.2011.1079].
Role of histone modifications in gastric cancer (Review).
Zhang Y, Wang L, Wang L … +7 more , Li Z, You R, Meng X, Gao Y, Zhu L, Wei S, Li M
Int J Oncol · 2026 May · PMID 41930465 · Full text
Histone modification is an important mechanism of epigenetic regulation. New histone modifications play key roles in the regulation of gene expression and in the development and progression of various diseases. In additi...
Histone modification is an important mechanism of epigenetic regulation. New histone modifications play key roles in the regulation of gene expression and in the development and progression of various diseases. In addition to histone modifications, epigenetic regulation includes classic pathways such as DNA methylation, chromatin remodeling complexes and non‑coding RNAs, which interact with each other and jointly shape the occurrence and development of gastric cancer (GC). The present study systematically elaborated on the role of histone modification in GC and introduced several main types of histone modification, including acetylation, methylation, citrullination, ubiquitination and lactylation, focusing on histone lactylation modification and exploring its biochemical basis, interaction with other modifications and functions such as metabolic reprogramming, cell proliferation, migration and immune escape, covering non‑tumor and other cancer fields. On this basis, the specific application of histone modification (acetylation, methylation and other modifications) in GC is further explained and the effects of histone lactylation on metabolic reprogramming, proliferation, migration and immune escape of GC are analyzed in detail. Finally, the clinical significance of histone lactylation modifications in the diagnosis and prognosis of GC, biomarkers, therapeutic targets and drug resistance mechanisms provides a reference for an in‑depth understanding of the role of histone modifications, especially lactylation modifications, in the development of GC and clinical transformation applications.
Hypoxia‑induced exosomal CAMTA1 promotes radio‑resistance in MDA‑MB‑231 cells by regulating NRG1 to mediate M2 macrophage polarization.
Li Q, Jiang M, Zhu B … +5 more , Wei W, Xia L, Huang J, Gao H, Du M
Int J Oncol · 2026 May · PMID 41891984 · Full text
Radiotherapy remains an irreplaceable treatment modality for breast cancer (BC). Calmodulin‑binding Transcription Activator 1 (CAMTA1) has been implicated in tumor progression; however, its role in BC is unclear. The pre...
Radiotherapy remains an irreplaceable treatment modality for breast cancer (BC). Calmodulin‑binding Transcription Activator 1 (CAMTA1) has been implicated in tumor progression; however, its role in BC is unclear. The present study aimed to elucidate the mechanistic function of CAMTA1 in BC. RNA sequencing was performed on RAW264.7 macrophages co‑cultured with 4T1 cells and subjected to X‑ray irradiation. , THP‑1 cells were co‑cultured with MDA‑MB‑231 cells under hypoxic conditions. Exosome morphology was observed under transmission electron microscopy and PKH67 staining was used to trace exosome uptake. Flow cytometry was used to detect CD163 expression while ELISA measured the levels of IL‑10 and IL‑12. Reverse transcription‑quantitative (RT‑q) PCR and immunoblotting analysis were used to detect the expressions of neuregulin 1 (NRG1), CAMTA1 and hypoxia‑inducible factor‑1α. Cell apoptosis, cell cycle distribution, cell viability and proliferation were evaluated using flow cytometry, MTT assay and colony formation assay. , transfected MDA‑MB‑231 cells were injected into BALB/c nude mice combined with radiotherapy and exosome injection. Histopathological changes in tumor tissues were examined using H&E staining. Immunohistochemistry analysis was performed to assess the expressions of NRG1, Caspase‑3 and CD163. RNA sequencing, RT‑qPCR and immunoblotting analysis revealed that NRG1 expression was markedly increased in RAW264.7 macrophages co‑cultured with 4T1 cells. NRG1 was found to be involved in M2 polarization induced by hypoxia‑treated MDA‑MB‑231 cells, which in turn promoted radio‑resistance. CAMTA1 expression was highly expressed in exosomes derived from hypoxic MDA‑MB‑231 cells and exosomal CAMTA1 promoted the M2 polarization of THP‑1 macrophages. , CAMTA1 overexpression greatly enhanced tumor growth, increased NRG1 expression, inhibited cell apoptosis and promoted M2 polarization of macrophages in tumor tissue. MDA‑MB‑231 cells were found to deliver CAMTA1 to macrophages via exosomes, leading to upregulation of NRG1 and induction of M2 polarization, thereby enhancing BC cells resistance to radiotherapy. These findings provided novel insights into the mechanisms underlying radio‑resistance in BC and identify exosomal CAMTA1 as a potential therapeutic target.
Selective antitumor and apoptosis‑inducing effects of the Src inhibitor PP1 in human tongue squamous cell carcinoma cells.
Kantibekovna SL, Wang S, Kang H … +2 more , Shin YM, Jang BC
Int J Oncol · 2026 May · PMID 41891963 · Full text
Src phosphorylation (activation) is associated with the proliferation and survival of numerous human cancer cells. The role of Src phosphorylation and expression, as well as its pharmacological inhibition by PP1, a Src i...
Src phosphorylation (activation) is associated with the proliferation and survival of numerous human cancer cells. The role of Src phosphorylation and expression, as well as its pharmacological inhibition by PP1, a Src inhibitor, in the growth of oral squamous cell carcinoma (OSCC), remain unclear. The present study explored whether Src is expressed and phosphorylated in HSC‑3 human oral cancer cells and whether PP1 treatment affects the proliferation of these cells. Src was found to be highly expressed and phosphorylated in HSC‑3 human oral cancer cells. Notably, treatment with PP1 at 10 µM significantly reduced cell proliferation and induced apoptosis, evidenced by DNA fragmentation, caspase‑9 and ‑8 activation, and poly(ADP‑ribose) polymerase cleavage. Mechanistically, PP1 not only inhibited Src phosphorylation but also disrupted a broad network of oncogenic pathways, including EGFR, JAK2, STAT‑3, PKB and ERK‑1/2 in HSC‑3 cells. Furthermore, PP1 induced markers of ER stress and inhibited protein translation, as shown by increased eIF‑2α phosphorylation and decreased S6 phosphorylation. The critical role of Src was confirmed by pharmacological inhibition and further validated when small interfering RNA‑mediated knockdown mimicked the anti‑proliferative effects of PP1. Importantly, these potent anticancer effects were conserved in another OSCC cell line (YD‑10B) and, were validated in vivo, where PP1 suppressed tumor growth in a zebrafish xenograft model. Collectively, these findings suggest that PP1 exerts strong anticancer effects on human oral cancer by simultaneously inhibiting Src activity and disrupting a network of associated oncogenic pathways (EGFR, STAT‑3, PKB and ERK‑1/2).
Multifaceted roles of miR‑124 in cancer: Molecular mechanisms and clinical prospects (Review).
Guo J, Guo Y, Chen P … +5 more , Xiao W, Tan Y, Wang Z, Lu Y, Yue X
Int J Oncol · 2026 May · PMID 41891957 · Full text
MicroRNAs (miRNAs or miRs) are a class of small non‑coding RNAs that are critical regulators of gene expression. By targeting messenger RNAs, they play essential roles in various biological processes, including developme...
MicroRNAs (miRNAs or miRs) are a class of small non‑coding RNAs that are critical regulators of gene expression. By targeting messenger RNAs, they play essential roles in various biological processes, including development, differentiation, immunity, metabolism and apoptosis. miRNA dysregulation is often associated with tumorigenesis and cancer progression. miR‑124, a miRNA predominantly and specifically expressed in the central nervous system, is commonly downregulated in various cancers. It inhibits multiple malignant traits, including tumor growth, metastasis, stemness and chemoresistance. Furthermore, miR‑124 influences the tumor microenvironment and modulates antitumor immune responses. These diverse functions highlight their significant potential for clinical application. Its expression is modulated by various upstream factors, including transcription factors, signaling pathways, epigenetic modifications, and other non‑coding RNAs. However, the precise mechanisms governing this upstream regulation require further investigation. Despite this, the translational application of miR‑124 for early cancer diagnosis and therapy faces several significant challenges, including improving its stability and bioavailability and developing effective delivery systems. The present study provides a comprehensive overview of the multifaceted roles of miR‑124 in cancer, elucidating its underlying molecular mechanisms and exploring its clinical potential. By synthesizing the current literature, it was aimed to consolidate the current understanding of miR‑124 and identify promising avenues for future research.
[Corrigendum] Epithelial protein lost in neoplasm‑α (EPLIN‑α) is a potential prognostic marker for the progression of epithelial ovarian cancer.
Liu R, Martin TA, Jordan NJ … +3 more , Ruge F, Ye L, Jiang WG
Int J Oncol · 2026 May · PMID 41860031 · Full text
Following the publication of the above article, an interested reader drew to the authors' attention that, regarding the cell invasion assay experiments shown in Fig. 5A on p. 2493, the 'WT' and 'pEF6' data panels were st...
Following the publication of the above article, an interested reader drew to the authors' attention that, regarding the cell invasion assay experiments shown in Fig. 5A on p. 2493, the 'WT' and 'pEF6' data panels were strikingly similar, albeit the coloration of the images differed slightly from each other, suggesting that these images were derived from the same original source. A second reader also noted that, concerning the scratch‑wound assay experiments shown in Fig. 6B, the images for the WT and pEF6 experiments at the 0 h (top panels) and 36 h (lower panels) time points contained overlapping sections (specifically, the 'WT/0 h' panel with the pEF6/0 h panel, and the 'WT/36 h' panel with the pEF6/36 h panel), suggesting that the two pairs of panels were likewise derived from the same original sources. Upon examining their original data, the authors realized that these figures had been inadvertently assembled incorrectly. Revised versions of Figs. 5 and 6, now showing the correct data for the 'WT' panel in Fig. 5A and the pEF/0 h and pEF/36 h panels in Fig. 6B, are shown on the next two pages. Note that the errors made in assembling these figures did not have a gross effect on the conclusions reported in this study. The authors thank the Editor of for granting them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 48: 2488‑2496, 2016; DOI: 10.3892/ijo.2016.3462].
Crosstalk between KRAS and miRNAs in pancreatic cancer: Opportunities for its diagnosis, prognosis and therapeutic intervention (Review).
Aloliqi AA, Alnuqaydan AM, Alshebremi M … +2 more , Rahmani AH, Khan AA
Int J Oncol · 2026 May · PMID 41860028 · Full text
Pancreatic cancer, predominantly manifested as pancreatic ductal adenocarcinoma (PDAC), is a highly aggressive malignancy in which the dysregulated crosstalk between Kirsten rat sarcoma viral oncogene homolog (KRAS) and...
Pancreatic cancer, predominantly manifested as pancreatic ductal adenocarcinoma (PDAC), is a highly aggressive malignancy in which the dysregulated crosstalk between Kirsten rat sarcoma viral oncogene homolog (KRAS) and microRNAs (miRNAs) plays a critical role. It is one of the leading causes of cancer‑related mortality worldwide, with its global incidence more than doubling over the past 25 years. PDAC is characterized by rapid progression, invasiveness and profound resistance to conventional therapies, resulting in dismal prognosis. Its genetic profile is characterized by activating KRAS mutations, present in ~90% of cases. These mutations act as molecular switches that activate multiple intracellular signaling cascades and transcription factors, promoting uncontrolled proliferation, survival, migration and transformation. In addition to direct KRAS alterations, dysregulation of KRAS‑targeting miRNAs further amplify aberrant RAS signaling. Emerging evidences highlights the significant role of miRNAs in driving tumor initiation, progression and metastasis. Several tumor‑suppressive miRNAs that regulate KRAS signaling have demonstrated the capacity to suppress pancreatic tumor development and in preclinical models. Despite these advances, miRNA‑based therapies, including mimics or anti‑miRNA oligonucleotides targeting KRAS, remain largely unexplored in patients with PDAC. Further, circulating miRNAs show promise as non‑invasive biomarkers for disease detection, monitoring progression and assessment of tumor aggressiveness. The present review provided a concise overview of KRAS signaling and its frequent mutations in PDAC, examines strategies to target KRAS and discussed the crosstalk between KRAS and tumor‑suppressive miRNAs in regulating pancreatic tumorigenesis. It further explored diagnostic and prognostic miRNAs in pancreatic cancer. Collectively, these insights underscored the potential of miRNA‑based interventions to improve early detection, prognosis and targeted therapy in this lethal disease.
Enolase 1: A paradigm of metabolic enzyme moonlighting in tumorigenesis (Review).
Ni X, Zhang M, Zhang K … +6 more , Wang C, Guo J, Fan W, Zheng L, Jiang T, Zhang G
Int J Oncol · 2026 May · PMID 41823547 · Full text
Enolase 1 (ENO1) plays a pivotal role in tumor development, recognized as a multifunctional oncogene across diverse cancers. Initially known for its central role in glycolysis, where it catalyzes the conversion of 2‑phos...
Enolase 1 (ENO1) plays a pivotal role in tumor development, recognized as a multifunctional oncogene across diverse cancers. Initially known for its central role in glycolysis, where it catalyzes the conversion of 2‑phosphoglycerate to phosphoenolpyruvate, the influence of ENO1 extends far beyond. Recent studies have unveiled its additional roles in promoting tumor progression through plasminogen receptor activity, nucleic acid binding activity and signaling functions. The function of ENO1 is intricately regulated by a wide array of post‑translational modifications, such as phosphorylation, ubiquitination, acetylation, methylation, succinylation and glycosylation. These modifications fine‑tune its enzymatic activity, stability and subcellular localization, thereby affecting tumor behavior. ENO1 holds significant diagnostic and prognostic value, with its expression levels closely linked to tumor malignancy and patient survival outcomes. In preclinical models, multiple therapeutic approaches targeting ENO1 have demonstrated tumor progression‑inhibiting effects. Consequently, drug development efforts centered on ENO1 are gaining momentum, with anticancer agents targeting this protein showing promising potential. As ENO1 emerges as a novel therapeutic target in oncology, the present review summarizes the latest research progress on ENO1 in the field of cancer.
[Corrigendum] Influence of MLH1 on colon cancer sensitivity to poly(ADP‑ribose) polymerase inhibitor combined with irinotecan.
Tentori L, Leonetti C, Muzi A … +8 more , Dorio AS, Porru M, Dolci S, Campolo F, Vernole P, Lacal PM, Praz F, Graziani G
Int J Oncol · 2026 May · PMID 41823545 · Full text
Following the publication of the above article, an interested reader drew to the attention of the Editorial Office that the immunofluorescence images shown in Fig. 3B on p. 214 to represent the 'HCT116 SiP' and 'HCT116+3...
Following the publication of the above article, an interested reader drew to the attention of the Editorial Office that the immunofluorescence images shown in Fig. 3B on p. 214 to represent the 'HCT116 SiP' and 'HCT116+3 SiP' experiments (top row of data) were strikingly similar. Upon examining their data, the authors have realized that the data in Fig. 3B were presented incorrectly; specifically, the data shown in the 'HCT116+3 SiP' panel were erroneously duplicated from the data shown correctly in the 'HCT116 SiP' panel. The authors have now submitted a revised version of Fig. 3, containing the corrected version of the 'HCT116+3 SiP' data panel in Fig. 3B, and this is shown on the next page. Note that this error 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 43: 210‑218, 2013; DOI: 10.3892/ijo.2013.1932].
Diverse roles of SERPINE1 in regulating cellular proliferation and invasion.
Wang W, Zhao P, Wang T … +4 more , Wu W, Li J, Huang Q, Mo J
Int J Oncol · 2026 May · PMID 41823537 · Full text
Serine protease inhibitor clade E member 1 (SERPINE1) is involved in various biological processes, but its role in promoting or suppressing tumorigenesis remains controversial. The present study focused on the effects of...
Serine protease inhibitor clade E member 1 (SERPINE1) is involved in various biological processes, but its role in promoting or suppressing tumorigenesis remains controversial. The present study focused on the effects of SERPINE1 downregulation on cell proliferation and invasion across three types of tumors to elucidate the underlying mechanisms. Based on data from an analysis of The Cancer Genome Atlas dataset, high SERPINE1 levels in patients with breast cancer and low‑grade glioma were associated with a poor prognosis, whereas elevated SERPINE1 expression in patients with skin cutaneous melanoma associated with improved outcomes. With respect to cell proliferation phenotypes, SERPINE1 knockdown increased xenograft growth and the proliferation of melanoma C918 cells by promoting cell cycle progression through the modulation of minichromosome maintenance complex component 3 and the activity of p53/SMAD3 regulators; conversely, SERPINE1 knockdown reduced the xenograft growth and proliferation of MDA‑MB‑231 breast cancer cells by decreasing the urokinase‑type plasminogen activator receptor‑mediated ERK/p38 activity ratio and similarly decreased proliferation in H4 glioma cells through an heat shock protein 90‑alpha (HSP90α)‑mediated reduction in the ERK/p38 activity ratio. Regarding invasion and metastasis, SERPINE1 knockdown consistently reduced invasion, matrix metalloproteinase (MMP) activity, and lung metastasis in both C918 and MDA‑MB‑231 cells but paradoxically increased invasion and MMP‑1 activity in H4 cells through the HSP90α‑p38‑MMP‑1 axis. Collectively, these findings suggested that SERPINE1 exerts diverse effects on cell proliferation and invasion through multiple regulatory mechanisms. These findings indicated that therapy targeting SERPINE1, which involves a comprehensive understanding of its diverse mechanisms of function, can increase treatment precision and reduce adverse reactions.
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