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, for the MTT assay experiments shown in Fig. 2A on p. 1655, the GDC‑0152/ANGPTL2 panel appeared to overlap with the ANGPTL2 panel, albeit the panel had been rotated through 180°; moreover, the magnification of the right‑hand panel was very different, creating an impression that the ANGPTL2 panel showed more cells. Upon analyzing the data independently in the Editorial Office, it came to light that that certain of the flow cytometric data in Fig. 2B and the nuclear staining experiments in Fig. 2C were strikingly similar to data in other articles written by different authors at different research institutes that had already been accepted for publication elsewhere. Owing to the fact that the contentious data in the above article had already been published prior to its submission to International Journal of Oncology, the Editor 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 46: 1651‑1658, 2015; DOI: 10.3892/ijo.2015.2872].

Ovarian cancer (OC) is the most lethal disease in women. Resistance to paclitaxel (PTX) is the main cause of treatment failure in patients with OC. The STAT1 protein is a transcription factor implicated in a variety of cellular processes. The present study explored the function and regulatory mechanism of STAT1 in the reversal of PTX resistance in vivo and in vitro. The OC cell lines SK‑OV‑3 and OVCAR‑3 and their counterpart PTX‑resistant OC cell lines SK3R‑PTX and OV3R‑PTX were applied. The Tet‑On STAT1‑overexpression plasmids were constructed using the technique of the Tet‑On gene expression system and were packaged by lentivirus. RNA and protein were detected by reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analysis, respectively. OC cell mRNA‑sequencing and subsequent RT‑qPCR verification revealed that STAT1 expression was downregulated in PTX‑resistant cells compared with their sensitive counterparts (P<0.01), except for STAT1β expression in SK3R cells (P>0.05). Cell viability was assessed using a CCK‑8 assay and PTX sensitivity was detected based on their IC₅₀ values. Overexpression of STAT1 sensitized PTX responses and decreased the tumor volume in xenograft mice. Bioinformatics analysis indicated that STAT1 had favorable effects on the overall survival of patients with OC. Apoptotic cells were detected using flow cytometry. STAT1α overexpression increased the percentage of apoptotic cells to 53.20±0.92 and 36.74±0.77% in OV3R‑PTX and A2780‑PTX cells, respectively, after 1 µM PTX treatment for 24 h. Mechanistically, overexpression of STAT1, especially STAT1α, confirmed by western blot and immunofluorescence staining, induced apoptosis by increasing apoptotic molecules such as Fas cell surface death receptor (FAS) and caspase‑8 (CASP8), which was abolished in the presence of a caspase blocker (Z‑VAD‑FMK). Furthermore, the dual‑luciferase assay confirmed that STAT1 directly bound to the promoter regions of the FAS and CASP8 genes. Thus, the present data demonstrated that STAT1 was a key mediator of the PTX chemotherapy response. Low STAT1 expression was a marker of PTX resistance, whereas overexpression of STAT1 sensitized OC cells to PTX and promoted apoptosis via the FAS/CASP8 signaling pathway. These findings may provide a potential therapeutic strategy to reverse PTX resistance in OC patients by targeting STAT1.

Following the publication of the above article, a concerned reader drew to the Editor's attention that, regarding the immunohistochemical staining experiments shown in Fig. 2, the insets for the data panels 2A and B, and 2C and D, respectively were remarkably similar, such that these data may not have consistently been identifiable with the main images proper for these figure parts. Secondly, with the western blot data shown in Fig. 3c, the PTCH1/Huh7 and ATAD2/siRNA‑HCCLM3 protein bands were remarkably similar, such that the same data were likely to have been duplicated in the figure where different experiments were intended to have been portrayed. Finally, the two sets of flow cytometric plots shown in Fig. 2A appeared to show similar groupings of dots, which would not have been anticipated if these experiments had been performed discretely under different experimental conditions, suggesting a fundamental flaw either in the way in which these experiments were performed, or in how the results were outputted. After having conducted an internal investigation of the data in this paper, the Editor of International Journal of Oncology has decided that this article should be retracted from the journal on the grounds of an overall lack of confidence in the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor sincerely apologizes to the readership for any inconvenience caused, and we thank the reader for bringing this matter to our attention. [International Journal of Oncology 45: 351‑361, 2014; DOI: 10.3892/ijo.2014.2416].

Hepatocellular carcinoma (HCC) is the predominant type of primary liver cancer, with high morbidity and mortality rates globally, ranking it among the leading causes of cancer‑related death worldwide. Despite notable advancements in HCC treatment in recent years, high rates of recurrence and treatment resistance remain significant clinical challenges. The development of drug resistance undermines the efficacy of current therapies and leads to poor patient outcomes. However, the specific role and detailed delivery mechanism of exosomal circular RNAs (circRNAs) in mediating this treatment resistance are still largely undefined. circRNAs represent a group of non‑coding RNAs with various biological roles. An increasing number of circRNAs are abnormally expressed in HCC and participate in the malignant progression of HCC, playing a role in HCC treatment resistance. Furthermore, circRNAs can exert additional effects when packaged into exosomes. Exosomes, as signaling molecules of intercellular communication, are enriched with circRNAs, which can be packaged, secreted and transferred to target recipient tumor cells, thereby regulating the development process and drug resistance of cancer. The present comprehensive review aims to summarize how these exosomal circRNAs regulate key hallmarks of cancer in HCC and critically synthesize the current literature, elucidating how exosomal circRNAs modulate therapeutic resistance in HCC and highlighting their potential as biomarkers and therapeutic targets.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the transfection experiments shown in Fig. 3 on p. 760, two pairs of data panels showed a surprisingly high level of similarity, such that the data appeared to have been derived from the same original sources where the results from differently performed experiments were intended to have been shown. The authors responded to the reader's concern by providing replacement data for Fig. 3; however, upon performing an independent analysis of the data in this paper in the Editorial Office, it was also noted that western blot data were overlapping in Fig. 4, and for the cell invasion assay experiments shown in Fig. 5, Fig. 5A and B were also found to contain overlapping data, albeit the level of brightness of the images differed. Owing to the large number of duplications of data, and other potential anomalies, that were 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 additional concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 46: 757-763, 2015; DOI: 10.3892/ijo.2014.2748].

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the first two lanes of the Actin blot in Fig. 1D looked strikingly similar to the Actin panels in Fig. 2E for the MDA‑MB‑231 cell line, In addition, the Actin panel in Fig. 4A (showing a time series) looked very similar to the Actin panel in Fig. 4B (showing different treatments). Upon analyzing the data independently in the Editorial Office, it came to light that there was an overlapping pair of data panels for the immunohistochemical data shown in Fig. 6C, such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original source, and data featured in Fig. 6D had subsequently appeared in a paper published in the journal Tumor Biology that was written by different authors at different research institutes. The authors were contacted by the Editorial Office to offer an explanation for these possible anomalies in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Oncology 48: 2479‑2487, 2016; DOI: 10.3892/ijo.2016.3483].

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the immunohistochemical data shown in Fig. 2B and C, the PBS/TUNEL panel in Fig. 2B appeared to be strikingly similar to the PBS/E1A panel shown in Fig. 2C. Furthermore, for the E1A experiments portrayed in Fig. 2C, portions of the data panels shown for the H101 and E1A groups also appeared to be strikingly similar, albeit with rotation of one of the panels. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 46: 1759‑1767, 2015; DOI: 10.3892/ijo.2015.2852].

Following the publication of the above paper, a potential problem regarding the presentation of the co‑localization experiments shown in Fig. 5A and C was brought to the Editor's attention by a concerned reader. Specifically, the Flotillin/gp91 co‑localization panels (Fig. 5A) appeared to be unexpectedly similar to the Flotillin/p22 panels (Fig. 5C), even though, according to the Materials and methods section, the different antibody treatments that were reported might have precluded the possibility of these images looking so similar. The authors were contacted by the Editorial Office to offer an explanation for this potential anomaly in the presentation of the data in this paper (or to clarify how the experiments had been performed), although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 37: 1483‑1493, 2010; DOI: 10.3892/ijo_00000801].

Transition‑metal nanoparticles (NPs) have been extensively studied owing to their unique physical and chemical properties, ability to form a variety of nanostructures and targeting properties. After surgery, chemotherapy, radiotherapy and targeted therapy, immunotherapy has emerged as a major strategy for cancer treatment. In particular, immune checkpoint inhibition has attracted much attention in preclinical and clinical applications. The combination of transition‑metal NPs with tumor immunotherapy offers great potential. Therefore, the present review focused on four major transition‑metal NPs (Au, Ag, Cu and Fe NPs) and their respective categories, presented their characteristics and roles in the biomedical field and discussed their potential toxicities. In addition, the mechanisms of action of different tumor immunotherapies and the applications of transition‑metal NPs in tumor immunotherapy are discussed. The current status of, and challenges associated, with the clinical transformation of transition‑metal NPs in tumor immunotherapy are described to provide ideas for the subsequent development and clinical application of transition‑metal NPs.

Obesity is a global epidemic strongly associated with increased breast cancer (BC) risk and mortality, particularly in postmenopausal women. Obesity‑induced chronic breast inflammation drives carcinogenesis via dysregulated adipokine signaling (leptin and adiponectin), insulin resistance, hyperinsulinemia and pro‑inflammatory cytokines (TNF‑α and IL‑6). These factors activate oncogenic pathways (NF‑κB and PI3K/AKT/mTOR pathways), which promote DNA damage, cell proliferation and immunosuppression. Clinically, obesity is associated with advanced tumor presentation, reduced treatment efficacy and poorer survival compared with those of normal‑weight patients with BC. Despite progress, the molecular interactions between obesity‑related inflammation and BC remain incompletely understood, and diagnostic/prognostic tools for obese patients require refinement. The present review synthesizes current evidence on obesity‑BC mechanisms and their clinical translation to inform prevention and precision oncology strategies.