International journal of oncology最新文献

Following the publication of the above article, an interested reader drew the authors' attention to the fact, for the wound‑healing assay data shown in Fig. 6 on p. 1632, the 'T16 h/p85 WT' and 'T16 h + RA/p85 D' panels appeared to contain an overlapping section, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. Upon contacting the authors, they realized that Fig. 6 had been inadvertently assembled incorrectly. The revised version of Fig. 6, now showing the correct data for the 'T16 h + RA/p85 D' panel, 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 International Journal of Oncology 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 40: 1627‑1635, 2012; DOI: 10.3892/ijo.2012.1383].

Breast carcinoma remains a major global health burden requiring innovative diagnostic and therapeutic strategies. Exosomal miRNAs have emerged as key factors in breast carcinoma that influence tumor progression, metastasis and treatment resistance. Recent studies have elucidated their mechanisms of action, including their roles in regulating oncogenic and tumor‑suppressive pathways, modulating the tumor microenvironment and promoting chemo‑resistance. Advances in miRNA‑based therapies such as miRNA mimics and inhibitors have shown promise in combination treatments, enhancing their therapeutic efficacy. Furthermore, exosomal miRNAs play a role in breast carcinoma calcification, offering novel insights into tumor progression. Unlike previous reviews that focus on a single function or therapeutic potential of miRNAs, the present review systematically integrated the multilevel role of exosomal miRNAs in breast cancer from the two dimensions of oncogenicity and tumor inhibition and the regulatory mechanism of breast carcinoma calcification and proposes that the exosomal miRNA calcification axis may be a key link connecting tumor metabolism and pathological calcification. Despite the potential of miRNAs, challenges remain in optimizing exosome isolation techniques and standardizing miRNA detection methods for clinical applications. Future research should focus on refining miRNA‑based liquid biopsies, developing delivery systems that target exosomes to enhance therapeutic efficacy and early detection strategies and ultimately improving patient survival and quality of life. The present review comprehensively explored the roles of exosomal miRNAs and highlighted their importance in breast carcinoma research. The present review illustrated the potential of exosomal miRNAs as non‑invasive biomarkers and therapeutic targets in precision medicine.

Kynurenine (Kyn) 3‑monooxygenase (KMO) is a key enzyme of the tryptophan (Try)‑Kyn pathway and is located on the outer membrane of mitochondria. Notably, it has not yet been elucidated as to whether KMO is involved in hepatocellular carcinoma (HCC) progression by affecting mitochondria. In the present study, KMO was revealed to be downregulated in HCC patients and this downregulation was associated with a poor prognosis. Notably, the downregulation of KMO promoted the proliferation and migration of HCC cells and increased mitochondrial mass. The levels of the Try metabolite 3‑hydroxyanthranilic acid (3‑HAA) were elevated in HCC cells overexpressing KMO. The results indicated that 3‑HAA may inhibit HCC cell growth promoted by KMO downregulation and reverse the KMO downregulation‑induced increase in mitochondrial mass. Furthermore, KMO and 3‑HAA were shown to regulate the expression of the transcription factor nuclear receptor subfamily 4 group A member 1 (NR4A1) and reduce NR4A1 mitochondrial translocation, thus inhibiting the growth of HCC cells. In summary, the current study elucidated that low KMO expression in HCC affects mitochondrial mass and function by reducing the level of the Try metabolite 3‑HAA, downregulating the expression of NR4A1 and promoting its mitochondrial translocation, which in turn may promote the progression of HCC. These findings provide new insights into the treatment of HCC, potentially targeting the mitochondria and the Try‑Kyn pathway.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the wound healing assay data shown in Fig. 2D, a pair of the data panels appeared to be overlapping, such that the data from the same original source had apparently been used to show the results of differently performed experiments. Furthermore, concerning the immunohistochemical data shown in Fig. 7A and C, similarly, two pairs of the data panels contained overlapping data, where the results of different experiments were intended to have been portrayed. Owing to the duplications of data 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 concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 41: 599‑610, 2012; DOI: 10.3892/ijo.2012.1496].

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell migration and invasion assay data shown in Fig. 5A on p. 1895 were strikingly similar to data in an article written by different authors at different research institutes that had already been accepted for publication in the journal OncoTargets and Therapy. 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 52: 1886‑1898, 2018; DOI: 10.3892/ijo.2018.4356]

Pancreatic ductal adenocarcinoma (PDAC) is the seventh leading cause of cancer‑related death worldwide in both men and women. While sex‑specific differences are increasingly recognized as critical determinants of health and disease, particularly in oncology, they remain markedly underexplored in PDAC. Emerging evidence suggests that sex differences influence numerous aspects of PDAC, including treatment response and prognosis. This knowledge gap represents a notable barrier to the development of effective, personalized therapeutic strategies for both sexes. The present review provides a comprehensive overview of the current knowledge on sex‑based differences in PDAC, encompassing epidemiology, risk factors, chemotherapy pharmacokinetics and toxicity, prognosis, therapeutic response, immune interactions, tumor microenvironment, tumor microbiota and molecular biomarkers.

Protein tyrosine phosphatase non‑receptor 18 (PTPN18) is widely expressed in breast cancer (BC) cell lines. Additionally, high levels of PTPN18 facilitate an improved overall survival and prognosis in patients with BC. However, the effects and mechanisms of PTPN18 in BC remain unclear. In the present study, it was found that PTPN18 serves a tumor suppressor role in BC cells by promoting apoptosis, inhibiting proliferation and metastasis and inducing cell cycle arrest. Bioinformatics analysis showed that PTPN18 was significantly negatively correlated with the cell cycle and downregulated cyclin E expression, which was consistent with the experimental results. Subsequent co‑immunoprecipitation assay results showed that PTPN18 could bind to cyclin E and promote its degradation through the ubiquitin‑proteasome pathway. Moreover, the addition of cyclin E2 did not reduce the binding of PTPN18 to cyclin E1. In the present study, the signaling pathways involved in cell cycle regulation were further investigated and it was found that PTPN18 may regulate the expression levels of cyclin‑dependent kinase (CDK) inhibitor 1A and CDK inhibitor 1B proteins through phosphatidylinositol 3‑kinase/protein kinase B signaling pathway, which leads to cell cycle arrest and tumor inhibition in BC. Thus, analysis of the tumor suppressor mechanism of PTPN18 not only helps us to understand its biological function but also provides a theoretical basis for the development of new therapeutic strategies for BC.

Circular RNAs (circRNAs) are associated with various biological features of cancer, including chemosensitivity and the structural characteristics of circRNAs indicate their potential as liquid biomarkers. Gemcitabine is a cornerstone treatment for pancreatic cancer (PC). A deeper understanding of gemcitabine sensitivity and the exploration of clinically valuable liquid biomarkers that are predictive of gemcitabine sensitivity may contribute to the development of improved‑tailored treatment strategies for PC. The aim of the present study was to identify a candidate circRNA associated with gemcitabine sensitivity, investigate its biological functions and evaluate its potential as a liquid biomarker in predicting gemcitabine sensitivity. circRNA sequencing analysis was conducted to identify candidate circRNAs and the function of a candidate circRNA in modulating gemcitabine sensitivity was investigated in vitro. Further, the potential of this circRNA in predicting gemcitabine sensitivity in patients with PC who received gemcitabine‑based neoadjuvant chemotherapy was evaluated using pre‑treatment serum samples. circ72309 was identified as the candidate circRNA and its overexpression in gemcitabine‑resistant PC cell lines increased gemcitabine‑induced apoptosis and markedly increased gemcitabine sensitivity in vitro. Furthermore, circ72309 decreased cytidine deaminase by increasing reactive oxygen species activity and increasing human equilibrative nucleoside transporter 1 expression via regulation of target miRNAs. Patients with high serum circ72309 had markedly improved progression‑free survival (PFS) and high serum circ72309 was an independent prognostic predictor of a favorable PFS in patients with PC. circ72309 affected multiple steps in the gemcitabine metabolic pathway and its overexpression resulted in markedly increased gemcitabine sensitivity. Therefore, circ72309 expression in the pre‑treatment serum samples may serve as a predictor of gemcitabine sensitivity in patients with PC.

Hypoxic tumor microenvironment (TME) is a common occurrence in the development of solid tumors, which activates hypoxia‑inducible factors (HIFs) and their downstream signaling pathways in cancer cells to facilitate tumor progression and immune escape. However, among the various immune cells that constitute innate and adaptive immune systems, HIFs have a more intricate function; moreover, different isoforms of HIFs play different functions under spatial and temporal conditions. HIFs are conducive to the adaptation of various immune cells to the hypoxic TME. The stability of HIF‑α can regulate metabolism and directly regulate the expression of immune genes. Additionally, the activation of HIF signaling may also inhibit the development of immune cells in some tumor environments, affecting the antigen recognition and killing processes to assist cancer cells in immune escape. Therefore, understanding the relationship between HIF signaling and immune cells more comprehensively may yield substantial benefits for the immunotherapy of various types of cancer. The present study reviewed the role of HIFs in immunity, including their role in T cells, B cells, macrophages, neutrophils, dendritic cells and natural killer cells. It also discussed the effectiveness of HIF targeted therapy in clinical application, the challenges associated with it and the development of a precise targeting drug delivery system. The present review may help researchers comprehend the tumor immune process in a hypoxic microenvironment. It aimed to offer novel strategies for cancer immunotherapy and prolonging the overall survival of patients.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that, in Fig. 6, the same data appeared to have been included in three of the flow cytometric plots featured in this figure (for the Non‑treated, Scrambled and SiRNAi BIK experiments). Moreover, the control β‑actin western blots in Figs. 2B, 4A and 8B appeared to be the same (although, in these cases, the lanes for the blots were labelled up identically, and so these apparent duplications may not have represented an incorrect assembly of these figures); similarly, the control blots in Fig. 7A and B were also matching. However, the control β‑actin western blots in three other figure parts (Fig. 1C and 7A/B) were also duplicated, and in this case, the numbers of lanes in the gel slices were different / the lanes were labelled differently. The authors were contacted by the Editorial Office to offer an explanation for these potential 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, the Editor of International Journal of Oncology has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 43: 1777‑1786, 2013; DOI: 10.3892/ijo.2013.2127].