Journal of Oncology
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Acceptance rate6%
Submission to final decision136 days
Acceptance to publication68 days
CiteScore3.900
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Aberrant Glycosylation in Pancreatic Ductal Adenocarcinoma 3D Organoids Is Mediated by KRAS Mutations

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 Journal profile

Journal of Oncology publishes research related to breast cancer, lung cancer, gastrointestinal cancer, skin cancer, head and neck cancer, paediatric oncology, neurooncology as well as genitourinary cancer.

 Editor spotlight

Chief Editor, Professor Bruno Vincenzi, is an Associate Professor of Medical Oncology at University Campus Bio-Medico, Italy. His research interests include urogenital neoplasms and the pathophysiology and treatment of bone metastases.

 Special Issues

We currently have a number of Special Issues open for submission. Special Issues highlight emerging areas of research within a field, or provide a venue for a deeper investigation into an existing research area.

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Research Article

Molecular Insights into the Breast and Prostate Cancer Cells in Response to the Change of Extracellular Zinc

Zinc dyshomeostasis is manifested in breast and prostate cancer cells. This study attempted to uncover the molecular details prodded by the change of extracellular zinc by employing a panel of normal and cancerous breast and prostate cell lines coupled with the top-down proteomics with two-dimensional gel electrophoresis followed by liquid chromatography-tandem mass spectrometry. The protein samples were generated from MCF-7 breast cancer cells, MCF10A normal breast cells, PC3 prostate cancer cells, and RWPE-1 normal prostate cells with or without exogenous zinc exposure in a time course (T0 and T120). By comparing the cancer cells vs respective normal epithelial cells without zinc treatment (T0), differentially expressed proteins (23 upregulated and 18 downregulated in MCF-7 cells; 14 upregulated and 30 downregulated in PC3 cells) were identified, which provides insights into the intrinsic differences of breast and prostate cancer cells. The dynamic protein landscapes in the cancer cells prodded by the extracellular zinc treatment reveal the potential roles of the identified zinc-responsive proteins (e.g., triosephosphate isomerase, S100A13, tumour proteins hD53 and hD54, and tumour suppressor prohibitin) in breast and prostate cancers. This study, for the first time, simultaneously investigated the two kinds of cancer cells related to zinc dyshomeostasis, and the findings shed light on the molecular understanding of the breast and prostate cancer cells in response to extracellular zinc variation.

Research Article

ARV-825 Showed Antitumor Activity against BRD4-NUT Fusion Protein by Targeting the BRD4

Objective. The bromodomain-containing 4 (BRD4) is a member of the bromodomain and extra terminal domain (BET) family, which is an important epigenetic reader. It is currently a promising oncology target. In some tumors, BET bromodomain inhibitors have demonstrated promising results. Proteolysis-targeting methods (PROTAC), which rapidly and effectively degrade BRD4, have displayed considerable potential in the treatment of tumors in recent years. The purpose of this study is to examine the potential impact of BRD4 PROTAC compounds ARV-825 on oncogene BRD4-NUT fused protein in NUT carcinoma. Methods. The effectiveness of ARV-825 was evaluated at the cellular level using the cell counting kit 8 test, wound healing, cell transfection, western blotting analysis, and RNA sequencing. The effectiveness of ARV-825 was also examined in vivo using a xenograft model. Results. The BRD4-NUT fusion gene was overexpressed in 3T3 cells, and the pathogenic fusion gene was simulated. The results showed that the overexpression of BRD4-NUT could promote the proliferation and migration of 3T3 cells, but the expression of BRD4 protein was degraded after the addition of the novel cereblon-based PROTAC compound ARV-825 against BRD4, resulting in inhibition of BRD4-NUT 3T3 cell proliferation and migration. Further RNA-seq analysis showed that overexpression of BRD4-NUT was accompanied by increased expression of gene (e.g., Myc, E2F, TRAFs, Wnt, Gadd45g, and Sox6) with significantly enriched pathway (e.g., small cell lung cancer, NF-kappa B signaling pathway, and breast cancer), promoted cell cycle from G 1 phase to S phase, and increased cell proliferation and migration, activated the antiapoptosisi signal, led to abnormal cell growth, and ultimately led to tumorigenesis. The addition of ARV-825 effectively rescued this process and effectively inhibited cell vitality, proliferation, and migration. In vivo studies demonstrated that treatment with ARV-825 greatly suppressed tumor growth without causing harmful side effects and downregulated the BRD4-NUT expression level. Conclusion. Through the induction of BRD4 protein degradation, ARV-825 can successfully limit BRD4-NUT 3T3 cell proliferation in vitro and in vivo. These findings suggested that the BRD4 inhibitor ARV-825 would be an effective therapeutic strategy for treating NUT carcinoma that with the genetic feature of BRD4-NUT fusion event.

Research Article

A Natural Organic Compound “Decursin” Has Both Antitumor and Renal Protective Effects: Treatment for Osteosarcoma

Osteosarcoma is a rare malignant tumor that commonly occurs in children. Anticancer drugs, for example, cisplatin, aid in postsurgery recovery but induce side effects such as renal damage, affecting the life prognosis of patients. Decursin which is one of the bioactive components has been reported for its anti-inflammatory, antioxidant, and antitumor effects, but the effect on osteosarcoma is unexplained. In this study, the research theme was to examine the sensitizing effect of decursin and its influence on cisplatin-induced nephrotoxicity. The cell viability and half maximal inhibitory concentration (IC50), apoptosis induction, and effect on cell cycle and Akt pathways were examined. In vivo, we examine the effects of decursin on tumors and mice bodies. Additionally, the effects of the cisplatin-decursin combination were evaluated in vitro and in vivo. Decursin suppressed cell viability and induced apoptosis via the cell cycle. Decursin also inhibited the Akt pathway by suppressing the phosphorylation of Akt. It enhanced apoptosis induction and lowered cell viability in combination with cisplatin. The increasing tumor volume was suppressed in the decursin-administrated group with further suppression in combination with cisplatin compared to sole cisplatin administration. The decrease in renal function and renal epithelial cell damage caused by cisplatin was improved by the combinatorial treatment with decursin. Therefore, decursin demonstrated an antitumor effect on the osteosarcoma cells and a renal protective effect in combination with cisplatin. Therefore, decursin is a prospective therapeutic agent against osteosarcoma.

Review Article

Histopathologic Patterns of Ovarian Tumors in Hawassa University Comprehensive Specialized Hospital, Southern Ethiopia

Objective. In Ethiopia, there is no national-level cancer registry except capital Addis Ababa, and little research was performed on ovarian tumors. This study is aimed at assessing different histopathologic patterns of ovarian tumors and their distribution based on age, biological behavior, and gross findings at a tertiary-level hospital in Ethiopia. Methods. In this study, 187 biopsy-confirmed ovarian tumors from September 2017 to August 2021 were included. All data were collected from the pathology department report format, classified according to the latest World Health Organization (WHO) classification system, and analyzed using SPSS 20.0 and Microsoft Excel 2010 at Hawassa University Comprehensive Specialized Hospital, Hawassa, Ethiopia. Results. A total of 187 women with ovarian tumors were included in this study. Of these, 143 (76.5%) were benign, 35 (18.7%) were malignant, and 9 (4.8%) were borderline tumors. Both benign and borderline tumors mostly occur at the age of 20–39 years. Surface epithelial tumors were the most common histopathologic pattern at 57.8% followed by germ cell tumors at 29.4% and sex cord-stromal tumors at 11.7%. Mature cystic teratomas were the most common benign ovarian tumors accounting for 37.8% of them, while serous cystadenocarcinomas were the most common malignant ovarian tumors accounting for 31.4% of malignant neoplasms. Conclusion. In the current study, surface epithelial tumors were the most common ovarian tumors followed by germ cell tumors. Younger age at presentation was observed for malignant ovarian tumors.

Research Article

miR-21 Targets ASPP2 to Inhibit Apoptosis via CHOP-Mediated Signaling in Helicobacter pylori-Infected Gastric Cancer Cells

Helicobacter pylori (H. pylori) infection affects cell survival pathways, including apoptosis and proliferation in host cells, and disruption of this balance is the key event in the development of H. pylori-induced gastric cancer (HPGC). H. pylori infection induces alterations in microRNAs expression that may be involved in GC development. Bioinformatic analysis showed that microRNA-21 (miR-21) is significantly upregulated in HPGC. Furthermore, quantitative proteomics and in silico prediction were employed to identify potential targets of miR-21. Following functional enrichment and clustered interaction network analyses, five candidates of miR-21 targets, PDCD4, ASPP2, DAXX, PIK3R1, and MAP3K1, were found across three functional clusters in association with cell death and survival, cellular movement, and cellular growth and proliferation. ASPP2 is inhibited by H. pylori-induced miR-21 overexpression. Moreover, ASPP2 levels are inversely correlated with miR-21 levels in HPGC tumor tissues. Thus, ASPP2 was identified as a miR-21 target in HPGC. Here, we observed that H. pylori-induced ASPP2 suppression enhances resistance to apoptosis in GC cells using apoptosis assays. Using protein interaction network and coimmunoprecipitation assay, we identified CHOP as a direct mediator of the ASPP2 proapoptotic activity in H. pylori-infected GC cells. Mechanistically, ASPP2 suppression promotes p300-mediated CHOP degradation, in turn inhibiting CHOP-mediated transcription of Noxa, Bak, and suppression of Bcl-2 to enact antiapoptosis in the GC cells after H. pylori infection. Clinicopathological analysis revealed correlations between decreased ASPP2 expression and higher HPGC risk and poor prognosis. In summary, the discovery of H. pylori-induced antiapoptosis via miR-21-mediated suppression of ASPP2/CHOP-mediated signaling provides a novel perspective for developing HPGC management and treatment.

Research Article

Fibroblast Growth Factor 11 Enables Tumor Cell Immune Escape by Promoting T Cell Exhaustion and Predicts Poor Prognosis in Patients with Lung Adenocarcinoma

Fibroblast growth factor 11 (FGF11) accelerates tumor proliferation in a variety of cancer types. This study aimed to examine the link between FGF11 and the prognosis of lung adenocarcinoma. FGF11 was searched in the Tumor Cancer Genome Atlas (TCGA) and ImmProt databases. The link between FGF11 and lung cancer clinical data was investigated using TCGA and Kaplan–Meier (KM)-plotter databases, and we developed a prediction model. Putative mechanisms of action were investigated using Gene Ontology (GO) and KEGG enrichment analyses. The GeneMANIA and STRING databases were used to search for genes that interact with FGF11, and the Tumor Immune Estimation Resource (TIMER) database was used to discover connections between FGF11 and immune cells, as well as any correlations with immune-related genes. We found that FGF11 expression was higher in the lung adenocarcinoma tissue than in the paracancerous tissue, and patients with high FGF11 expression had a lower overall survival, progression-free survival, and disease specific survival rate than those with low FGF11 expression. The expression of FGF11 was inversely linked to six types of infiltrating immune cells in the TIMER database and was associated with EGFR, VEGFA, BRAF, and MET expressions. The FGF11 gene is negatively correlated with the expression of most immune cells, mainly with various functional T cells including Th1, Th1-like, Treg, and Resting Treg characterization genes. These results indicate that FGF11 has the potential to be a new lung adenocarcinoma biomarker. It increases tumor cell immune escape by boosting T cell exhaustion in the tumor microenvironment, contributing to the poor prognosis of the patients with lung adenocarcinoma. These results provide incentive to further research FGF11 as a possible biomarker and drug target for patients with lung adenocarcinoma.

Journal of Oncology
 Journal metrics
See full report
Acceptance rate6%
Submission to final decision136 days
Acceptance to publication68 days
CiteScore3.900
Journal Citation Indicator-
Impact Factor-
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