Oncology reports最新文献

Endometrial cysts of the ovary (EMC) may develop into endometriosis (EM)‑associated ovarian cancer over time (EAOC), but the pathogenesis of this disease has not been determined. In the present study, RNA sequencing was used to identify a feasible biomarker, and the molecular function of this biomarker in eutopic endometrial cells from EAOC and EMC patients was evaluated to explore the potential mechanism related to EAOC and orthotopic endometrial tissue. RNA sequencing was performed on 5 EAOC and 4 EMC tissue samples, and differential expression analysis was performed. To identify biomarkers, differentially expressed genes were subjected to protein‑protein interaction network design, Gene Ontology pathway enrichment, and Gene Set Enrichment Analysis pathway enrichment. The expression of FOS in the endometrium was detected via immunohistochemical staining. Lv‑FOS was utilized to upregulate FOS in human endometrial stromal cells (hEnSCs), and Cell Counting Kit‑8, colony formation and scratch assays were performed to assess cell viability, proliferation and migration, respectively. Western blotting was used to determine protein expression. In total, 249 genes, including FOS, were differentially expressed. Pathway enrichment analysis demonstrated that the MAPK, AP‑1, ERK and other signaling pathways were involved in the EMC‑to‑EAOC conversion. FOS upregulation in hEnSCs increased cell viability, proliferation and migration. Western blot results revealed that after FOS expression was inhibited, P21 expression was upregulated, and CDK4, Cyclin D1, p‑Stat3, MMP2 and MMP9 expression was downregulated. In conclusion, mitosis and the cell cycle were found to affect the progression of EMC to EAOC. The expression of FOS, a novel biomarker, was identified to enhance the malignant potential of eutopic endometrial stromal cells in patients with EM‑associated ovarian cancer.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that certain discrete western blot data shown in the RT‑qPCR blots in Figs. 1A and 2A, and western blot data in Fig. 5 were strikingly similar to data that had already appeared in previously published papers in different journals written by different authors at different research institutes. Furthermore, some of the protein bands featured in the western blots in Figs. 1C, 2C and 4 were strikingly similar to other bands within the same figures, suggesting that the figures in question may have undergone inappropriate editing. Having considered the issues identified, the Editor of Oncology Reports has decided that this article should be retracted from the Journal on account of the re‑use of previously published data and the uncertainties regarding the presentation of data in Figs. 1C, 2C and 4. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 30: 3032‑3038, 2013; DOI: 10.3892/or.2013.2785].

Glioblastoma (GBM) is the most aggressive primary brain tumour, characterised by high heterogeneity, aggressiveness and resistance to conventional therapies, leading to poor prognosis for patients. In recent years, with the rapid development of molecular biology and genomics technologies, significant progress has been made in understanding the molecular mechanisms of GBM. This has revealed a complex molecular network involving aberrant key signalling pathways, epigenetic alterations, interactions in the tumour microenvironment and regulation of non‑coding RNAs. Based on these molecular features, novel therapeutic strategies such as targeted therapies, immunotherapy and gene therapy are rapidly evolving and hold promise for improving the outcome of GBM. This review systematically summarises the advances in molecular mechanisms and therapeutic approaches for GBM. It aims to provide new perspectives for the precise diagnosis and personalised treatment of GBM, and to ultimately improve the prognosis of patients.

Prostate cancer (PCa) is second only to lung cancer in terms of death among men worldwide. Advanced PCa frequently results in bone metastases, which occur in ~90% of patients and frequently result in severe skeleton‑related events. Currently, the treatment for this disease is limited to alleviating its clinical symptoms and cannot provide a complete cure. Therefore, the development of novel treatment strategies is particularly important. In recent years, numerous novel strategies for the diagnosis and treatment of PCa have emerged, resulting in good clinical efficacy. For example, strategies targeting prostate specific membrane antigen, poly ADP‑ribose polymerase and programmed cell death protein 1 have been applied to PCa‑induced bone metastasis, and have shown initial efficacy and great potential. Therefore, understanding the molecular mechanisms underlying the formation of bone metastases in patients with PCa is of importance for the effective management of this disease. The purpose of the present review is to comprehensively outline the roles of protein‑coding genes and non‑coding RNAs in the development of bone metastases of PCa to elucidate their significance in the management of PCa. The aim is to offer clinicians and researchers a comprehensive understanding of this topic.

Subsequently to the publication of the above paper, an interested reader has drawn to our attention that five pairs of data panels in Fig. 3A and B, showing the results of Transwell invasion and migration assay experiments, were overlapping, such that data which were intended to show the results from a number of differently performed experiments had apparently been derived from the same original sources. Following an independent assessment of these data in the Editorial Office, the Editor of Oncology Reports has decided that this article should be retracted from the publication on account of a lack of confidence in the integrity of 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 by the retraction of this article.[Oncology Reports 38: 1005‑1012, 2017; DOI: 10.3892/or.2017.5759].

Despite advancements and refinements in the therapeutic approaches for hepatic malignancies, liver cancer remains a prevalent and deadly form of cancer, with its grim outlook posing as a significant clinical challenge. Phillyrin (PHN) has been reported to have anticancer effects, but the anticancer mechanism in liver cancer is ominous. By searching the potential target of PHN in the online database and liver cancer disease database, it was found that there is only one overlap gene, and DNA topoisomerase II alpha (TOP2A) is abnormally expressed in liver cancer tissues. TOP2A overexpression and downregulated hepatocellular carcinoma cell lines were then constructed in vitro, and it was examined whether PHN treatment induced ferroptosis in hepatocellular carcinoma by regulating TOP2A's inhibition of Janus kinase 2/Signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway through phenotypic assay, western blot assay, reverse transcription‑quantitative PCR assay and electron microscopy. The results showed that PHN could inhibit the expression of TOP2A protein and JAK2/STAT3 signaling pathway in hepatoma cells. PHN could also downregulate glutathione peroxidase 4 by suppressing the expression of TOP2A protein. PHN impeded the activity of factor inhibiting hypoxia‑inducible factor 1 alpha, thereby augmenting the synthesis of iron‑dependent apoptosis‑related proteins including cytochrome c oxidase subunit II, long‑chain acyl‑CoA synthetase family member 4 and NADPH oxidase 1, thus facilitating an increase in Fe²⁺ concentration and accelerating oxidative harm within hepatocellular carcinoma cells, culminating in the induction of ferroptotic cell death in these liver malignancy cells.

Following the publication of the above article, an interested reader drew to the authors' attention that the RT‑PCR data panels shown in Fig. 3C, showing the effects of PBIT and PBI‑Se treatment on endogenous IL‑8 mRNA expression levels in CaCo₂ cells, contained issues. Specifically, on p. 956, a pair of the β‑actin bands in the bottom panel of Fig. 3C were strikingly similar to those featured in the upper panel. Upon examining their original data, the authors realized that the bottom β‑actin panel in Fig. 3C had inadvertently been assembled incorrectly. Moreover, a typo was also identified in the Fig. 3C legend. The revised version of Fig. 3, showing the correct data for the β‑actin bands in the bottom panel in Fig. 3C, and now accurately displaying the correct images for the IL‑8 mRNA and β‑actin expression experiments, is shown on the next page. Additionally, the typo in the Fig. 3C legend has been corrected to read as follows: 'PBI‑Se (1‑4 µM) and PBIT (30‑60 µM) treatment reduced endogenous IL‑8 mRNA expression in CaCo₂ cells'. Note that the revisions made to this figure do not affect the overall results or the conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [Oncology Reports 30: 952‑960, 2013; DOI: 10.3892/or.2013.2483].

Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents. Histone acetyltransferases (HATs), such as p300, CBP and PCAF, modulate numerous biological processes, including cellular proliferation and oncogenesis, through histone acetylation. In the present study, it was investigated whether the curcumin analogs such as pentagamavunon‑1 (PGV‑1) and chemoprevention curcumin analog‑1.1 (CCA‑1.1) could target p300 and suppress OS. Computational analysis indicated that PGV‑1 and CCA‑1.1 bind to the HAT domain of p300. Accordingly, these analogs efficiently inhibited the HAT activity of p300 in vitro and promoted OS cell apoptosis, accompanied by downregulation of acetylated histone H3 at Lys‑27 and phosphorylated oncogenic STAT3 at Tyr‑705. Finally, it was found that PGV‑1 and CCA‑1.1 but not PGV‑1, significantly attenuates the growth of OS developed on the chicken egg chorioallantoic membrane (CAM). Collectively, the present results strongly suggest that curcumin analog‑mediated targeting of p300 might provide a clue to develop an effective treatment strategy against patients with OS.

As cancer incidence and mortality rates continue to rise, the urgency for research in this field has increased globally. Sideroflexin 1 (SFXN1), a pivotal member of the SFXN protein family, serves a crucial role in transporting serine to mitochondria and participates in one‑carbon metabolism, thereby influencing cell proliferation and differentiation. While SFXN1 is linked to lung cancer and glioma, its role in other malignancies remains largely unexplored. Utilizing The Cancer Genome Atlas, Human Protein Atlas, Gene Expression Profiling Interactive Analysis and University of Alabama at Birmingham Cancer Data Analysis Portal databases, the present study investigated the expression patterns, prognostic implications and association with immune cell infiltration of SFXN1. The present findings revealed that SFXN1 was differentially expressed across various tumor types, and exhibited significant associations with clinicopathological features and patient prognosis. Through immune infiltration analysis, a significant correlation between SFXN1 and T cells, B cells and immune checkpoint genes was established in numerous tumor types. Notably, loss‑of‑function experiments demonstrated that silencing of SFXN1 decreased cell proliferation, migration and invasion, while simultaneously increasing apoptosis in lung adenocarcinoma cells. Collectively, these findings suggested that SFXN1 expression could potentially serve as a biomarker for tumor diagnosis and prognosis, also emerging as a novel therapeutic target in cancer immunotherapy. The present study highlights the critical role of SFXN1 in cancer biology and paves the way for future translational efforts aimed at leveraging its potential in clinical oncology.

The ErbB/HER family of protein‑tyrosine kinases and PI3K represent crucial targets in the treatment of head and neck squamous cell carcinoma (HNSCC). A combination therapy of afatinib (ErbB inhibitor) and copanlisib (PI3K inhibitor), both Food and Drug Administration‑approved kinase inhibitors, can suppress the growth of human papillomavirus (HPV)‑positive HNSCC. The current study further evaluated the efficacy and clinical potential of this combination therapy for the treatment of HPV‑negative HNSCC in vitro and in vivo. Sulforhodamine B cell viability assay and Annexin V/propidium iodide staining demonstrated that this combination treatment markedly enhanced inhibition of cell viability and reduced cell survival when compared with treatment with either inhibitor alone in two HPV‑negative HNSCC cell lines. Notably, this combination also led to significant inhibition of xenograft tumor growth in mice, without any apparent effects on body weight. Western blot analysis found that copanlisib alone effectively blocked PI3K/Akt signaling but caused upregulation of HER2 and HER3 phosphorylation, as reported in other types of cancer. However, the combination of copanlisib and afatinib completely blocked phosphorylation of the ErbB family (including HER3) and Akt, while also increasing apoptosis. In conclusion, these results suggested that co‑targeting the ErbB family kinases and PI3K using a combination treatment of afatinib and copanlisib may have clinical potential for patients with HPV‑negative HNSCC.