International journal of oncology最新文献

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 International Journal of Oncology 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].

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 International Journal of Oncology 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].

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.

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.

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.

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.

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 Oncotarget (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 International Journal of Oncology 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].

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.

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 International Journal of Oncology 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].

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: RAD51, the eukaryotic recombinase and PALB2, a scaffolding protein. Their structural and functional roles are explored in the context of breast and ovarian cancer. RAD51 facilitates homology search and strand invasion, while PALB2 links BRCA1 and BRCA2, stabilizing RAD51 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 RAD51 and PALB2 mutations, focusing on risk stratification, PARP inhibitor efficacy and emerging therapies. Additionally, it highlighted the potential of RAD51 and PALB2 as biomarkers and therapeutic targets, contributing to advances in personalized cancer management.