Abstract
BackgroundEpithelial ovarian cancer (EOC) is the main subtype of ovarian cancer and shows an aggressive phenotype and poor prognosis. Neuronal pentraxin II (NPTX2) is a member of the neuronal pentraxin family and plays a contradictory role in different tumors. However, there has been no report about the possible role and effect of NPTX2 in EOC.MethodsBioinformatics analysis, qPCR, western blotting and immunohistochemistry were used to detect the expression of NPTX2 in EOC. Lentivirus-based transfection for NPTX2 overexpression or knockdown was performed on the EOC cell lines A2780, HEY, SKOV3 and OVCAR-3. The effect of NPTX2 on the malignant phenotype of EOC was examined through methods of MTS assay, Edu assay, transwell assay, western blotting analysis, qPCR analysis, luciferase reporter assay and xenograft experiment.ResultsEOC tissues showed higher NPTX2 expression than the normal tissues with poor prognosis. NPTX2 overexpression can promote the proliferation, invasion, migration and tumorigenesis of EOC via IL6-JAK2/STAT3 signaling pathway. Moreover, hypoxia-inducible factor-1(HIF-1) can promote the transcription and expression of NPTX2 under the hypoxic environment. NPTX2 knockdown abolished the hypoxia-induced malignant phenotypes in ECO.ConclusionsThe above results suggest that NPTX2 may play a novel role in ovarian cancer’s malignant phenotype and act as a promising treatment target for EOC molecular therapy.
Highlights
Ovarian cancer is one of the most common malignant tumors in females with the worst prognosis, accounting for 3.4% of all the female malignant tumors and 4.4% of female cancer deaths [1]
We performed Kaplan-Meier survival analysis for the prognostic significance of NPTX2 expression in ovarian carcinoma patients, and the survival time of patients with high NPTX2 expression was significantly lower in the TCGA dataset than in patients with low expression (Figure 1D)
After NPTX2 knockdown, the increase in proliferation of epithelial ovarian cancer (EOC) induced by hypoxic treatment was abolished (Figures 7A–C). Both the transwell and migration assays showed that hypoxic treatment promoted the invasion and migration of EOCs, while NPTX2 knockdown abolished these effects (Figures 7D, E). These findings suggested that NPTX2 can mediate the hypoxia-induced epithelial ovarian carcinoma malignant phenotype and NPTX2 can reverse these effects
Summary
Ovarian cancer is one of the most common malignant tumors in females with the worst prognosis, accounting for 3.4% of all the female malignant tumors and 4.4% of female cancer deaths [1]. Epithelial ovarian cancer (EOC) is the main subtype of ovarian cancer and shows a more aggressive phenotype than nonepithelial cancers [2]. Surgery combined with chemotherapy has achieved a certain effect, the patients’ longterm prognosis is not ideal. It has been reported that the 5-year survival rate is only 29% in the advanced stage of EOC patients [3]. Molecular targeted therapy is regarded as one of the most promising therapies for EOC treatment [4]. Epithelial ovarian cancer (EOC) is the main subtype of ovarian cancer and shows an aggressive phenotype and poor prognosis. Neuronal pentraxin II (NPTX2) is a member of the neuronal pentraxin family and plays a contradictory role in different tumors. There has been no report about the possible role and effect of NPTX2 in EOC
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