BackgroundPatients with ovarian cancer commonly have a poor prognosis, owing to its invasiveness and distant metastasis. Studies have found TM4SF1 participates in regulating tumor cell invasion and migration. Therefore, it is expected to become a target for anti-invasion and metastasis in ovarian cancer.MethodsThe expression of TM4SF1 in normal ovarian epithelial tissues, benign ovarian tumor tissues, primary foci of epithelial ovarian cancer and the matched lymph mode metastatic foci was detected using immunohistochemistry to analyze its association with prognosis. The expression of TM4SF1 in HO8910PM, SKOV3 was inhibited using RNAi, and the growth, proliferation, migration, invasion abilities of HO8910PM and SKOV3 cells and the growth of xenograft tumors in nude mice were examined.Results(1) The positive expression rate of TM4SF1 protein in epithelial ovarian cancer tissues (90.90%) was higher than that in benign ovarian tumor tissues (65.22%) and normal ovarian epithelial tissues (31.25%), and both differences were significant (P < 0.05). The expression of TM4SF1 protein was positive in all metastatic lymph node foci and matched primary foci (100%). (2) The level of TM4SF1 protein expression was positively correlated with the International Federation of Gynecology and Obstetrics (FIGO) stage and histological grade. However, The positive TM4SF1 protein expression was not an independent factor of prognosis (P > 0.05). (3) Silencing TM4SF1 expression did not affect growth, proliferation, or cell cycle distribution but inhibited the migration and invasion abilities of HO8910PM and SKOV3 cells. Silencing TM4SF1 expression inhibited the growth of xenograft tumors in nude mice.ConclusionTM4SF1 is a potential target for anti-invasion and metastasis in ovarian cancer.

The dysregulation of arrestin domain containing 3 (ARRDC3) has an important effect on oncogenesis and tumor progression in many cancers, including renal cell carcinoma and breast cancer. However, the role of ARRDC3 in ovarian cancer (OC) has not been reported. Methods: The present study explored the diagnostic and prognostic roles of ARRDC3 in ovarian cancer using GEPIA, ONCOMINE, GEO, and Kaplan-Meier Plotter databases for training and validation. Then, we conducted a stratified analysis for clinicopathological factors using Kaplan-Meier Plotter and GEPIA databases. To further explore the mechanisms, we also used the MIST database to visualize the protein-protein interaction network of ARRDC3 associated with OC. The gene-gene interaction network was visualized by GeneMANIA plugin in Cytoscape 3.8.0 software, and the associated co-expression genes of ARRDC3 were analyzed by the cBioPortal database. The 100 top co-expression genes chosen for gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used by the DAVID website. Results: A significant difference in ARRDC3 mRNA expression was found between OC and normal ovary tissues. ARRDC3 could potentially be implicated in the diagnosis of OC. A high ARRDC3 mRNA expression level was associated with poor overall survival and progression-free survival. However, no significance was reported in respect to post progression survival. Except for histology, which had no prognostic value for PPS in stratified analysis, stratified analysis of other factors had prognostic value for OS, PFS, and PPS. Interestingly, we found a positive correlation between ARRDC3 expression and CD8+ T cells, macrophages, neutrophils, and dendritic cells, indicating that ARRDC3 might be associated with immune infiltration of these immune cells. Coexpression genes enrichment analysis found that they were involved in the Renin-angiotensin system pathway. Conclusion: Differentially expressed ARRDC3 might be a potential prognostic and diagnostic marker in Ovarian Cancer.

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Objective:To investigate the clinical value of heart rate deceleration capacity (DC) in predicting the risk of epirubicin-induced cardiotoxicity.Methods:The CK-MB and cTnI levels and DC values of 86 patients were examined before chemotherapy and again after 2 and 4 cycles of chemotherapy. Patients were divided into low-risk group (LRG) (40 cases), medium-risk group (26 cases), and high-risk group (HRG) (20 cases) based on the calculated DC values.Results:After 4 cycles of chemotherapy, HRG showed a significantly greater increase in serum CK-MB (17.1 ± 4.9 vs. 14.6 ± 3.7) and cTnI (1.28 ± 0.38 vs. 1.0 ± 0.29) concentrations over the prechemotherapy levels when compared with LRG. After 2 and 4 cycles of chemotherapy, HRG exhibited a significantly greater increase in mean heart rate (2 cycles: 79.6 ± 6.0 vs. 77.6 ± 6.7; 4 cycles: 88.2 ± 10.2 vs. 82.4 ± 6.2) and the supraventricular (2 cycles: 68.9 ± 19.3 vs. 57.2 ± 17.6; 4 cycles: 131.1 ± 29.5 vs. 91.7 ± 16.5) and ventricular arrhythmia counts (2 cycles: 179.0 ± 20.5 vs. 162.3 ± 16.3; 4 cycles: 228.6 ± 44.8 vs. 187.4 ± 22.6) over the prechemotherapy values compared with LRG. When the supraventricular and ventricular arrhythmia counts measured after 4 cycles of chemotherapy were compared with those obtained before chemotherapy, HRG (131.1 ± 29.5 and 228.6 ± 44.8, respectively) showed the largest differences, followed by medium-risk group (107.4 ± 31.9 and 202.0 ± 29.8, respectively) and then LRG (91.7 ± 16.5 and 187.4 ± 22.6, respectively) (P < 0.01). After 4 cycles of chemotherapy, the incidence rates of ventricular arrhythmia greater than Lown's grade 3 (30% vs. 2.5%), QTc (20% vs. 0) elongation, and ST-T (40% vs. 5%) changes in HRG were significantly higher than those observed in LRG (P < 0.05).Conclusions:DC test was shown to be an effective predictor of the risk of epirubicin-induced cardiotoxicity.