International journal of oncology最新文献

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. In vivo 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 in vivo. 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.

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].

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.

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.

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.

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 in vivo was discussed. Finally, current translational bottlenecks were identified and future design considerations to achieve clinically viable, precision‑targeted nanomedicines for brain tumors were outlined.

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 International Journal of Oncology 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].

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.