International Journal Of Oncology[JOURNAL]
Sun
200 papers
[Expression of Concern] MicroRNA‑195 targets VEGFR2 and has a tumor suppressive role in ACHN cells via PI3K/Akt and Raf/MEK/ERK signaling pathways.
Sun P, Wang L, Lu Y … +7 more , Liu Y, Li L, Yin L, Zhang C, Zhao W, Shen B, Xu W
Int J Oncol · 2025 Nov · PMID 40849802 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the Transwell migration and invasion assay data shown in Fig. 3A and B, two pairs of panels appea...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the Transwell migration and invasion assay data shown in Fig. 3A and B, two pairs of panels appeared to contain overlapping sections of data (out of a total of ten panels), 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, a third pair of data panels in the same figure were found to be similarly affected. 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: 1155‑1163, 2016; DOI: 10.3892/ijo.2016.3608].
Lp‑PLA2 in the cancer landscape: From molecular mechanisms to therapeutic potential (Review).
Yang X, Tu Y, Liang N … +4 more , Li L, Zhang J, Xu J, Li C
Int J Oncol · 2025 Nov · PMID 40849801 · Full text
Lipoprotein‑associated phospholipase A2 (Lp‑PLA2), an important member of the phospholipase A2 superfamily, was originally investigated for its proinflammatory role in cardiovascular diseases. Recent studies have reveale...
Lipoprotein‑associated phospholipase A2 (Lp‑PLA2), an important member of the phospholipase A2 superfamily, was originally investigated for its proinflammatory role in cardiovascular diseases. Recent studies have revealed its significant role in tumorigenesis: It can act as either a tumor promoter or a tumor suppressor depending on the context. The present review systematically outlined the dual mechanisms by which Lp‑PLA2 contributes to cancer pathogenesis. As a tumor promoter, it promotes cancer progression via the induction of epithelial‑mesenchymal transition, glutathione peroxidase 4‑mediated resistance to ferroptosis, and vascular endothelial growth factor‑-dependent angiogenesis; conversely, as a tumor suppressor, it inhibits tumor growth by suppressing the Wnt/β‑catenin pathway in breast cancer gene 1‑mutated cancers or by promoting apoptosis. Mechanistic investigations clarify the interactions between Lp‑PLA2 and critical oncogenic pathways, such as the Notch and HIF1α pathways, while emphasizing the functional dichotomy that is influenced by the microenvironment. Current evidence supports the development of microenvironment‑guided targeting strategies and the potential value of Lp‑PLA2 as a prognostic biomarker and therapeutic target. These findings contribute to a theoretical framework for comprehending the context‑dependent roles of Lp‑PLA2 and may guide the development of innovative therapeutic approaches.
[Expression of Concern] ETS‑1: A potential target of glycolysis for metabolic therapy by regulating glucose metabolism in pancreatic cancer.
Zhang X, Wu D, Aldarouish M … +3 more , Yin X, Li C, Wang C
Int J Oncol · 2025 Oct · PMID 40808345 · 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. 4B and 5B, the AMPK panel in Fig. 4B looked strikingly similar t...
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. 4B and 5B, the AMPK panel in Fig. 4B looked strikingly similar to the ATG5 panel in Fig. 5B, and the p‑AMPK panel in Fig. 4B looked highly similar to the ATG7 panel in Fig. 5B. 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 50: 232-240, 2017; DOI: 10.3892/ijo.2016.3770].
From mitochondrial dysregulation to ferroptosis: Exploring new strategies and challenges in radioimmunotherapy (Review).
Wang T, Zhou X, Yin X … +8 more , Zhang A, Fan Y, Chen K, Tao H, Tang Z, Zhang P, He X, Yin L
Int J Oncol · 2025 Sep · PMID 40776761 · Full text
Ferroptosis is an iron‑dependent, lipid peroxidation‑driven form of regulated immunogenic cell death (ICD). ICD has demonstrated potential to overcome resistance to conventional cancer therapies, enhancing the efficacy o...
Ferroptosis is an iron‑dependent, lipid peroxidation‑driven form of regulated immunogenic cell death (ICD). ICD has demonstrated potential to overcome resistance to conventional cancer therapies, enhancing the efficacy of treatments such as chemotherapy, radiotherapy, immunotherapy and photodynamic therapy. Notably, in the context of radiotherapy, ferroptosis serves a key role, particularly when combined with radioimmunotherapy. Mitochondria are central to the regulation of radiation‑induced oxidative stress and the remodeling of the immune microenvironment, and they undergo characteristic morphological changes during the ferroptotic process. However, the precise regulatory association between mitochondrial dysfunction and ferroptosis remains incompletely understood, and there is an ongoing debate regarding this complex interaction. The present review aimed to explore the mechanisms through which mitochondria and ferroptosis interact in the context of radiotherapy, with a focus on how ferroptosis exacerbates mitochondrial dysfunction. Additionally, the present review proposed novel strategies leveraging radioimmunotherapy to offer more precise and effective approaches for cancer treatment.
A perspective on the chemical structures and molecular mechanisms of curcumin and its derivatives and analogs in cancer treatment (Review).
Zhu L, Wang Y, Wang Q
Int J Oncol · 2025 Sep · PMID 40776760 · Full text
Curcumin is a polyphenolic nutraceutical compound, which has a variety of pharmacological properties that may prevent or treat cancer, chronic inflammation, depression, anxiety and nerve damage. However, due to the poor...
Curcumin is a polyphenolic nutraceutical compound, which has a variety of pharmacological properties that may prevent or treat cancer, chronic inflammation, depression, anxiety and nerve damage. However, due to the poor solubility of curcumin in water and instability, it has limited applications. Therefore, a series of curcumin derivatives or analogs have been designed and synthesized to optimize the physicochemical and therapeutic properties and pharmacokinetic features of curcumin. Curcumin derivatives or analogs have been shown to possess beneficial biochemical effects, thus have been considered as potential medications. The present review summarized the structural characteristics and classification of available curcumin derivatives or analogs, and described the molecular mechanisms of curcumin and its derivatives as potential pharmaceutical drugs in various types of cancer, such as lung, prostate, breast and colorectal cancer. The present review also discussed the adverse effects and limitations of curcumin and its derivatives/analogs in preclinical and clinical trials. Analysis of the existing studies on curcumin may potentially contribute to the design and synthesis of innovative curcumin derivatives or analogs as drugs and tools in therapeutic, preventative and diagnostic medical applications in associated diseases.
Cancer‑associated fibroblasts in human malignancies, with a particular emphasis on sarcomas (Review).
Benesova I, Kalkusova K, Kwon YS … +8 more , Taborska P, Stakheev D, Krausova K, Smetanova J, Ozaniak A, Bartunkova J, Smrž D, Strizova ZO
Int J Oncol · 2025 Oct · PMID 40776758 · Full text
Over the course of the last 10 years, clinical oncology has seen significant changes. Although there has been much interest in targeting cancer cells with immunotherapy, the initial enthusiasm has waned as clinical trial...
Over the course of the last 10 years, clinical oncology has seen significant changes. Although there has been much interest in targeting cancer cells with immunotherapy, the initial enthusiasm has waned as clinical trial results have not met the initial expectations, especially for solid tumors. As a result, research efforts are now shifting towards the study of other cells in the tumor microenvironment. Cancer‑associated fibroblasts (CAFs) are one of the main adversarial cell types that help cancer cells to resist oncological treatment. However, although CAFs have been extensively studied in different types of carcinomas, their role in sarcomas remains poorly understood. Despite this topic being of especial importance, to the best of the authors' knowledge, no literature review currently addresses and summarizes the up‑to‑date knowledge on the role of CAFs in sarcomas. The present review article aimed to address this literature gap by summarizing our current understanding of CAFs in carcinomas and integrating this information with what is currently known about CAFs in sarcomas. The review also suggested novel approaches for targeting CAFs, and outlines new avenues for identifying novel therapeutic targets, which may markedly impact future research in this field.
Cuproptosis in prostate cancer: Molecular mechanisms, prognostic biomarkers and therapeutic frontiers of cuproptosis‑related genes (Review).
Long Z, Chang Y, Zhu K … +2 more , Chen Z, You Y
Int J Oncol · 2025 Sep · PMID 40776742 · Full text
Prostate cancer (PCa) is among the most prevalent malignancies in males globally and management remains complex. In recent years, cuproptosis, an emerging form of cell death, has offered novel insights for PCa treatment....
Prostate cancer (PCa) is among the most prevalent malignancies in males globally and management remains complex. In recent years, cuproptosis, an emerging form of cell death, has offered novel insights for PCa treatment. Cuproptosis refers to a copper‑mediated cellular death mechanism that is intricately associated with mitochondrial metabolism, with cuproptosis‑related genes (CRGs) exerting a notable effect on both cuproptosis and PCa. CRGs and other cuproptosis‑associated indicators have demonstrated efficacy as prognostic predictors of PCa and these predictors may exhibit potential as novel therapeutic targets in the treatment of PCa. The mechanisms underlying cuproptosis in PCa remain to be fully elucidated; thus, further research is required to validate the expression patterns of CRGs and their associated indicators and examine the potential association with the characteristics, treatment responses and prognoses of patients with PCa. The present study aimed to investigate novel therapeutic strategies that may enhance the prognosis and quality of life of patients with PCa.
[Retracted] MicroRNA‑181a regulates epithelial‑mesenchymal transition by targeting PTEN in drug‑resistant lung adenocarcinoma cells.
Li H, Zhang P, Sun X … +4 more , Sun Y, Shi C, Liu H, Liu X
Int J Oncol · 2025 Oct · PMID 40776740 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the scratch wound and cell migration and invasion assay experiments shown in Fig. 2A and B and Fi...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the scratch wound and cell migration and invasion assay experiments shown in Fig. 2A and B and Fig. 5A‑C, a large number of data panels showed evidence of overlapping data, both within the same figure parts and comparing between figures. Similarly, evidence was also uncovered of data duplication comparing the cell microscopic images in Figs. 6A, 7B and 8B. Owing to the large number of data duplication events that have been identified in this paper, the Editor of has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 47: 1379‑1392, 2015; DOI: 10.3892/ijo.2015.3144].
Inhibiting SSBP1 enhances ferroptosis and improves the effectiveness of sorafenib treatment for liver cancer.
Li S, Yang X, Gao H … +7 more , Hu X, Wang D, Zhang Q, Xu J, Zhang J, Zhu L, Wang Z
Int J Oncol · 2025 Sep · PMID 40747667 · Full text
Liver cancer is the third leading cause of cancer‑related mortality globally, with increasing morbidity and mortality rates. Sorafenib, a multi‑kinase inhibitor, is an effective first‑line therapy for late‑stage liver ca...
Liver cancer is the third leading cause of cancer‑related mortality globally, with increasing morbidity and mortality rates. Sorafenib, a multi‑kinase inhibitor, is an effective first‑line therapy for late‑stage liver cancer. However, its effectiveness is hindered by low responsiveness, high drug resistance and significant side effects. The progression and metastasis of liver cancer are associated with alterations in mitochondrial metabolism, including mitochondrial stress responses and defects in oxidative phosphorylation, which are involved in the increased production of reactive oxygen species. Targeting mitochondrial biogenesis and bioenergetics presents a promising therapeutic strategy. Bioinformatics analysis (integrated analysis of The Cancer Genome Atlas, mitochondrial genomes, liver cancer mouse models, and bioinformatics tools) revealed that the expression of single‑stranded DNA‑binding protein 1 (SSBP1) was significantly elevated in liver cancer. In addition, MTT and colony formation assays showed that increased SSBP1 expression notably enhanced cell proliferation, while wound healing and Transwell assays demonstrated enhanced metastasis. Furthermore, flow cytometry, qPCR, and western blotting indicated that SSBP1 knockout impaired mitochondrial function and increased sensitivity to sorafenib, effectively attenuating cancer progression. Clinical correlation analysis demonstrated that higher SSBP1 expression was associated with poorer prognosis in patients with liver cancer. In summary, the present study identified SSBP1 as a potential driver of tumor growth and a promising prognostic biomarker and therapeutic target in liver cancer, thus providing novel insight for improving patient outcomes.
Knockdown of ACC1 promotes migration and invasion of U251 glioma cells by epigenetically suppressing SDH.
Wei X, Wang Y, Zhao W … +4 more , Yang W, Tang J, Zhao B, Liu Y
Int J Oncol · 2025 Sep · PMID 40747663 · Full text
Glioma is a common and aggressive malignant brain tumor. Despite advances in research, the mechanisms driving glioma initiation and progression remain incompletely understood. The present study aimed to assess the role o...
Glioma is a common and aggressive malignant brain tumor. Despite advances in research, the mechanisms driving glioma initiation and progression remain incompletely understood. The present study aimed to assess the role of acetyl‑CoA carboxylase 1 (ACC1) in glioma, focusing on its mechanistic function in U251 cells and its clinical significance. ACC1 expression was first assessed in four glioma cell lines and then the effects on cellular functions were evaluated. Based on the finding that ACC1 knockdown altered the phenotype of U251 cells, potentially through modulation of succinate dehydrogenase (SDH) activity, further mechanistic assessments were performed. Finally, the association between ACC1 expression and patient prognosis was analyzed. The results demonstrated that ACC1 overexpression inhibited proliferation, migration and invasion in U87 cells. Conversely, ACC1 knockdown promoted these processes in U251, T98G and LN229 cells. Mechanistically, in U251 cells, ACC1 knockdown increased acetyl‑CoA levels, enhancing substrate availability for P300. This led to upregulation of DNA methyltransferase 1 (DNMT1), hypermethylation of the SDH promoter and subsequent SDH downregulation. The resulting increase in reactive oxygen species (ROS) levels promoted U251 cell migration and invasion. Analysis of clinical data revealed a significant correlation between low ACC1 expression and poor survival outcomes in patients with glioma. These findings suggest that ACC1 functions as a tumor suppressor in glioma. Its downregulation promotes a pro‑tumorigenic phenotype via the acetyl‑CoA/P300/DNMT1/SDH/ROS pathway, highlighting its potential as a prognostic marker and therapeutic target. This underscores the importance of developing personalized treatment strategies targeting ACC1 in glioma.
[Corrigendum] IL‑21R functions as an oncogenic factor and is regulated by the lncRNA MALAT1/miR‑125a‑3p axis in gastric cancer.
Yan L, Zhang J, Guo D … +3 more , Ma J, Shui SF, Han XW
Int J Oncol · 2025 Sep · PMID 40747659 · Full text
Following the publication of the above article, an interested reader drew to the authors' attention that their paper was found to contain data with a previous article that had been published in the journal (Figs. 2C and...
Following the publication of the above article, an interested reader drew to the authors' attention that their paper was found to contain data with a previous article that had been published in the journal (Figs. 2C and 4B), and in a paper that appeared subsequently in the journal Molecular Cancer. All cases involved the sharing of Transwell assay data, and the other papers in question were published by the same authors/the same research group. After having examined their original data, the authors realized that Figs. 2 and 4 had been inadvertently assembled incorrectly in the above paper. Specifically, Figs. 2C and D, and 4B and D, showing the results of Transwell assay experiments indicating the effects of IL‑21R knockdown or co‑transfection with IL‑21R and miR‑125a mimic on cell invasion in HGC‑27 and MKN‑45 cell lines, contained erroneous images. The revised versions of Figs. 2 and 4, featuring replacement data for Figs. 2C and D and 4B and D, showing the correct data obtained for the effects of IL‑21R knockdown or co‑transfection with IL‑21R and miR‑125a mimic on cell invasion, are shown on the next page. All authors confirm that the errors made in Figs. 2C and D and 4B and D did not influence the final conclusions reported in the above article, and they thank the Editor of for granting them the opportunity to publish a Corrigendum. All the authors agree to the publication of this Corrigendum, and apologize for the inconvenience to the readers. [International Journal of Oncology 54: 7‑16, 2019; DOI: 10.3892/ijo.2018.4612].
Novel non‑metal‑based contrast agents for MR imaging: Emerging approaches and clinical perspectives (Review).
Du T, Luo H, Song H … +2 more , Lin T, Yu Q
Int J Oncol · 2025 Aug · PMID 40682851 · Full text
Magnetic Resonance Imaging (MRI) relies on contrast agents to enhance image quality and diagnostic accuracy. Traditional metal‑based agents, such as gadolinium compounds, raise safety concerns due to potential toxicity a...
Magnetic Resonance Imaging (MRI) relies on contrast agents to enhance image quality and diagnostic accuracy. Traditional metal‑based agents, such as gadolinium compounds, raise safety concerns due to potential toxicity and long‑term retention in the body. The present review examines recent advancements in non‑metal‑based MRI contrast agents, focusing on fluorine‑19 (19F) compounds, chemical exchange saturation transfer (CEST) agents, nitroxide radicals, and hyperpolarized carbon agents. It discussed the mechanisms by which these agents improve contrast, including their biocompatibility and ability to provide molecular and metabolic information. Key findings highlight the high specificity of19F agents due to negligible background signals, the capacity of CEST agents for molecular imaging without metals, nitroxide radicals' utility in redox‑sensitive imaging, and hyperpolarized C compounds' role in real‑time metabolic assessment. Despite challenges such as low sensitivity and technical complexities, these non‑metal‑based agents offer promising, safer alternatives with enhanced diagnostic capabilities, paving the way for more precise and personalized medical imaging.
[Corrigendum] Dual targeting of glioblastoma multiforme with a proteasome inhibitor (Velcade) and a phosphatidylinositol 3‑kinase inhibitor (ZSTK474).
Lin L, Gaut D, Hu K … +3 more , Yan H, Yin D, Koeffler PH
Int J Oncol · 2025 Sep · PMID 40682846 · Full text
Following the publication of the above article, an interested reader drew to the attention of the Editorial Office that GAPDH bands featured for the U87 cell line (left‑hand panels) in Fig. 5 on p. 561 were strikingly si...
Following the publication of the above article, an interested reader drew to the attention of the Editorial Office that GAPDH bands featured for the U87 cell line (left‑hand panels) in Fig. 5 on p. 561 were strikingly similar to the GAPDH bands for the U118 cell line (right‑hand panels) shown in Fig. 1 on p. 559, even though the experiments shown in these figures were performed under different experimental conditions. Upon examining their data, the authors have realized that Fig. 5 was presented incorrectly; specifically, the cell lines ('U87' and 'U118') in Fig. 5 were mistakenly labeled in reverse, and the GAPDH bands from the right‑hand panels of Fig. 1 were inadvertently re‑used in the left‑hand panels of Fig. 5. The authors have now corrected the cell line labels and replaced the GAPDH bands in the left‑hand panels of Fig. 5 with alternative data from a repeated experiment. The revised version of Fig. 5 is shown below. It is important to 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 deeply apologize to the readership for any inconvenience caused. [International Journal of Oncology 44: 557‑562, 2014; DOI: 10.3892/ijo.2013.2205].
Role of exosomal non‑coding RNAs in cancer‑associated fibroblast‑mediated therapy resistance (Review).
Li J, Huang Y, Fu L … +7 more , Shi M, Hu G, Du F, Wang Z, Xiao Y, Zhang Y, Li Y
Int J Oncol · 2025 Aug · PMID 40682844 · Full text
Cancer‑associated fibroblasts (CAFs) represent an important component of the stromal cell population within the tumor microenvironment (TME) and are intricately linked to tumor growth, metastasis and drug resistance. In...
Cancer‑associated fibroblasts (CAFs) represent an important component of the stromal cell population within the tumor microenvironment (TME) and are intricately linked to tumor growth, metastasis and drug resistance. In the TME, non‑coding RNAs present in exosomes act as essential mediators of intercellular communication. Exosomal RNAs derived from cancer cells activate CAFs, which in turn regulate cancer cell proliferation, invasion and drug resistance. Conversely, exosomal RNAs derived from CAFs contribute to therapeutic resistance in cancer by modulating survival signaling pathways, epithelial‑mesenchymal transition, programmed cell death, drug transporter expression levels and immune evasion. The present review examines the role and mechanisms of exosomal RNAs in CAF‑mediated cancer therapeutic resistance and offers recommendations for future research based on the underlying mechanisms of CAF‑induced drug resistance.
[Corrigendum] STAT3 activation in HER2‑overexpressing breast cancer promotes epithelial‑mesenchymal transition and cancer stem cell traits.
Chung SS, Giehl N, Wu Y … +1 more , Vadgama JV
Int J Oncol · 2025 Aug · PMID 40682842 · Full text
Following the publication of the above article, a pair of interested readers drew to the Editor's attention that certain of the western blotting data featured in Figs. 1A and 3A were strikingly similar to data that had a...
Following the publication of the above article, a pair of interested readers drew to the Editor's attention that certain of the western blotting data featured in Figs. 1A and 3A were strikingly similar to data that had appeared in a pair of articles published previously by the same research group. Subsequently, an independent investigation of the data in this paper on the part of the Editorial Office revealed that a pair of the panels showing the results of cell invasion assays in Fig. 4A on p. 405 for the MCF7‑WT cells appeared to contain overlapping sections, such that data which were intended to show results from entirely different microscopic fields had apparently been derived from partly the same original field of view. Upon investigating these matters with the authors, they were able to repeat the experiments concerned (in the case of Figs. 1 and 3). The revised versions of Figs. 1, 3 and 4, now featuring the replacement data for Figs. 1A and 3A and the two completely differentiated microscopic fields of view for Fig. 4, are shown on the next two pages. The authors regret that certain of the data featured in Figs. 1 and 3 of this article were erronoeusly re‑used from a pair of their previous publications, and 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 44: 403‑411, 2014; DOI: 10.3892/ijo.2013.2195].
[Corrigendum] Dual roles of protein tyrosine phosphatase kappa in coordinating angiogenesis induced by pro-angiogenic factors.
Sun PH, Chen G, Mason M … +2 more , Jiang WG, Ye L
Int J Oncol · 2025 Aug · PMID 40641136 · Full text
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that the data for the PTPRK blots shown in Fig. 1B on p. 1129 were strikingly similar to data that had already appea...
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that the data for the PTPRK blots shown in Fig. 1B on p. 1129 were strikingly similar to data that had already appeared in a previous publication by the same authors in the journal . The authors have re‑examined their original data, and realize how this error occurred. The revised (and corrected) version of Fig. 1, now showing the correct data for the PTPRK blots in Fig. 1B, is shown below. The authors sincerely apologize for the error made in assembling this figure, although they confirm that this did not grossly affect either the results or the conclusions reported in this study. They also thank the Editor of for granting them the opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused. [International Journal of Oncology 50: 1127-1135, 2017; DOI: 10.3892/ijo.2017.3884].
MicroRNA‑21: A potential therapeutic target in lung cancer (Review).
Li Z, Zhang H, Chen Z … +3 more , Wu G, Guo W, Li Y
Int J Oncol · 2025 Aug · PMID 40641110 · Full text
In this review, the role of microRNA‑21 (miRNA‑21) as an oncogene in lung cancer was investigated. Studies have shown that miRNA‑21 can promote the progression of lung cancer by targeting downstream target genes, and its...
In this review, the role of microRNA‑21 (miRNA‑21) as an oncogene in lung cancer was investigated. Studies have shown that miRNA‑21 can promote the progression of lung cancer by targeting downstream target genes, and its expression can be modulated by transcription factors, DNA methylation or competitive endogenous RNA as an upstream regulator. This review highlights that miRNA‑21 can promote the progression of lung cancer through multiple signaling pathways, with a focus on the PI3K/AKT, MEK/ERK, TGF‑β/SMAD, Hippo, NF‑κB and STAT3 signaling pathways. Mechanistically, miRNA‑21 plays an important role in the progression of lung cancer by regulating multiple biological processes, such as proliferation, invasion, metastasis, apoptosis and angiogenesis in lung cancer cells. Higher expression of miRNA‑21 is associated with chemotherapy, radiotherapy and immune resistance in lung cancer. Targeting these molecular pathways may be a novel therapeutic strategy for treating lung cancer. Additionally, miRNA‑21 can serve as a biomarker for lung cancer diagnosis, prognosis and treatment response. This review also summarized the following: i) Current methods employed to inhibit the expression of miRNA‑21 in lung cancer, including CRISPR/Cas9 technology; ii) the application of natural anticancer agents, oligonucleotides, small molecules and miRNA sponges; and iii) the nano‑delivery systems developed for miRNA‑21 inhibitors. Finally, the advancements in research on miRNA mimics and inhibitors in clinical trials, which may promote the application of miRNA‑21 in clinical trials in lung cancer, were discussed. Given that lung cancer is a considerable public health challenge, these studies provide new ways of treating patients with lung cancer.
The role of abnormal epigenetic regulation of small GTPases in glioma (Review).
Zhang M, Huang Y, Zhang Q … +3 more , Zhang X, Kang L, Wang J
Int J Oncol · 2025 Aug · PMID 40613212 · Full text
Brain tumors are one of the most severe types of malignant tumors and glioma accounts for ~80% of malignant brain tumors. The current treatment methods for glioma are limited and patients with glioma often experience rel...
Brain tumors are one of the most severe types of malignant tumors and glioma accounts for ~80% of malignant brain tumors. The current treatment methods for glioma are limited and patients with glioma often experience relapse following treatment, which leads to a poor prognosis for these patients. Therefore, novel therapeutic targets and methods urgently need to be explored. The present review screened studies that mainly focused on the epigenetic regulation of small guanosine triphosphate (GTP)ase in glioma. These small GTPases participate in most cellular biological processes, including differentiation, proliferation, cell migration, apoptosis, vesicle and organelle dynamics and transport, nuclear dynamics and cytoskeleton regulation. Due to the diversity and importance of the biological functions of small GTPases, an increasing number of studies have focused on them; however, the incidence of changes in the gene structure of small GTPases is considered to be low in glioma. Several studies have shown that the abnormal expression of genes encoding small GTPases is often influenced by epigenetic regulation in glioma. Epigenetic regulation is a dynamic and reversible process, which implies that the reversal of abnormal epigenetic modifications is a potential treatment strategy for glioma. These previous studies, which are summarized in the present review, not only provide new therapeutic targets and prognostic markers, but also provide information regarding the treatment of glioma. The current review may provide valuable insights for future research and promote the clinical translation of relevant research results.
[Corrigendum] Metastasis suppressor 1 expression in human ovarian cancer: The impact on cellular migration and metastasis.
Liu R, Martin TA, Jordan NJ … +3 more , Ruge F, Ye L, Jiang WG
Int J Oncol · 2025 Aug · PMID 40613202 · Full text
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the cell invasion assays shown in Fig. 5A on p. 1436, the 'WT' and 'pEF6' data panels contained a...
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the cell invasion assays shown in Fig. 5A on p. 1436, the 'WT' and 'pEF6' data panels contained apparently overlapping sections of data, such that these experiments were apparently derived from the same original source where the results of differently performed experiments were intended to have been portrayed. After re‑examining their original data, the authors have realized that the data panel in Fig. 5A for the 'pEF6' experiment was inadvertently selected incorrectly. The revised version of Fig. 5, showing all the correct data for Fig. 5A, is shown on the next page. 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 47: 1429‑1439, 2015; DOI: 10.3892/ijo.2015.3121].
and in precision oncology: Clinical implications for HRD associated breast and ovarian cancers (Review).
Kausar MA, Alshammari KF, Alenazi F … +8 more , Anwar S, Khalifa AM, Ginawi T, Asiri A, Najm MZ, Rabbani SA, El-Tanani M, Gantayat S
Int J Oncol · 2025 Aug · PMID 40613200 · Full text
Maintaining genomic stability is essential for reducing the risk of carcinogenesis. Homologous recombination (HR) is a high‑fidelity DNA repair mechanism that addresses double‑strand breaks and interstrand crosslinks. Th...
Maintaining genomic stability is essential for reducing the risk of carcinogenesis. Homologous recombination (HR) is a high‑fidelity DNA repair mechanism that addresses double‑strand breaks and interstrand crosslinks. The present review examined two key components of HR: , the eukaryotic recombinase and , a scaffolding protein. Their structural and functional roles are explored in the context of breast and ovarian cancer. facilitates homology search and strand invasion, while links and , stabilizing filaments. Mutations in these genes compromise HR, increasing susceptibility to various cancers and impacting treatment efficacy by impairing DNA repair. The present review discussed the clinical implications of and mutations, focusing on risk stratification, PARP inhibitor efficacy and emerging therapies. Additionally, it highlighted the potential of and as biomarkers and therapeutic targets, contributing to advances in personalized cancer management.
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