Long non-coding RNA SNHG1 is an unfavorable prognostic factor and promotes cell proliferation and migration by Wnt/ß-catenin pathway in epithelial ovarian cancer.

Long non-coding RNAs (lncRNA) have been shown to serve critical roles in human cancers development, including epithelial ovarian cancer (EOC). Here, we identified a novel lncRNA SNHG1, which was markedly upregulated in human EOC tissues and cell lines. High SNHG1 expression was associated with aggressive clinical features and poor prognosis of EOC patients. Moreover, the downregulation of SNHG1 remarkably inhibited the EOC cells proliferation, migration and invasion, suppressed S-phase entry in vitro, and repressed tumor growth in vivo. In contrast, overexpression of SNHG1 could promote the aggressive behaviors of EOC cells. Furthermore, through western blot, we found that SNHG1 enhanced the expression of several downstream genes in Wnt/ß-catenin pathway. Our findings demonstrated that the dysregulation of SNHG1 is implicated in EOC tumorigenesis and progression through regulating Wnt/ß-catenin pathway.

Different effects of H2O2 treatment on cervical squamous carcinoma cells and adenocarcinoma cells.

INTRODUCTION: This study aims to compare the antioxidant abilities of cervical squamous carcinoma cells and cervical adenocarcinoma cells and to study the related mechanisms. MATERIAL AND METHODS: Cervical squamous carcinoma and adenocarcinoma cells were treated with H2O2. Cell proliferation was determined with the MTT assay. The reactive oxygen species (ROS) level was detected by the 2',7'-dichlorofluorescein-diacetate (DCFH-DA) method. The 5,5'-dithiobis-2-nitrobenzoic acid (DTNB) method was performed to measure intracellular concentrations of reduced glutathione (GSH) and oxidized glutathione (GSSG). The nitrite formation method, the molybdate colorimetric method, and the DTNB colorimetric method were used to determine activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), respectively. RESULTS: Compared with untreated control cells, cell proliferation of cervical squamous carcinoma cells and cervical adenocarcinoma cells was significantly inhibited by H2O2 treatment (p < 0.05). Reactive oxygen species levels and GSSG levels were significantly increased (p < 0.01), whereas GSH levels were significantly decreased (p < 0.05 or 0.01) in both cells after H2O2 treatment. Thus the ratio of GSH/GSSG was significantly decreased by H2O2 treatment in both cells (p < 0.01). In addition, H2O2 treatment significantly increased activities of SOD, CAT, and GPx in both cells (p < 0.05 or 0.01). Furthermore, the above-mentioned changes induced by H2O2 treatment were more dramatic in cervical squamous carcinoma cells. CONCLUSIONS: The antioxidant ability of cervical squamous carcinoma cells is lower than that of cervical adenocarcinoma cells, which may be related to the increased ROS levels in cervical squamous carcinoma cells induced by H2O2 treatments.