RESUMO
PURPOSE: LncRNA SOX2OT plays protective roles in high glucose-induced injuries, suggesting its potential involvement in diabetes. Therefore, we analyzed the role of SOX2OT in gestational diabetes mellitus (GDM). METHODS: A total of 216 pregnant women with a gestational age of about 2 months were enrolled in this study. The 216 pregnant women were monitored until delivery to record the occurrence of GDM. Adverse events, including miscarriage, premature delivery, intrauterine distress, intrauterine death, intrauterine infection, fetal malformation, macrosomia, and hypertension, were recorded. RESULTS: Two hundred sixteen pregnant women were divided into high and low SOX2OT level groups (n=108), with the median plasma SOX2OT level on the day of admission as the cutoff value. It was observed that the incidence of GDM was higher in the high SOX2OT level group (40/108) than in the low SOX2OT level group (12/108). Moreover, the SOX2OT expression level was higher in GDM patients than in non-GDM participants, and ROC curve analysis showed that plasma SOX2OT levels on the day of admission could separate potential GDM patients from the rest participants. Importantly, higher incidences of miscarriage, premature delivery, intrauterine distress, intrauterine death, intrauterine infection, fetal malformation, macrosomia, and hypertension were observed in the high SOX2OT group compared to the low SOX2OT group. CONCLUSION: SOX2OT is highly expressed in GDM and is closely correlated with multiple adverse events.
RESUMO
BACKGROUND: Golgi phosphoprotein 3 (GOLPH3) is a novel oncogene overexpressed in several human cancers, but specific contributions to endometrial carcinoma (EC) have not been examined. The aims of this study were to evaluate the GOLPH3 expression in EC and investigate its functions in EC cell proliferation, migration, and survival. METHODS: The expression levels of GOLPH3 in EC patient samples and EC cell lines (HEC-1A, KLE, RL95-2, and Ishikawa) were examined using qRT-PCR, western blotting and immunohistochemistry. Further, EC cell lines with either ectopic GOLPH3 overexpression or knockdown were established, and the effects on proliferation, apoptosis, invasion, and migration were investigated in vitro using cell viability and transwell assays and in mice following cell injection. RESULTS: Compared to adjacent non-cancerous tissues, expression of GOLPH3 was significantly upregulated in EC tissues (P< 0.05), and the expression level of GOPLPH3 was related to the grade of the tumor (P< 0.05). The expression of GOLPH3 was also higher in all four EC cell lines than endometrial stromal cells (ESCs) (P< 0.05). Moreover, GOLPH3 expression was greater in EC cell lines with high invasive capacity than in non-invasive EC cells (P< 0.05). Knockdown of GOLPH3 inhibited EC cell proliferation and increased cell apoptosis in vitro. Further, knockdown of GOLPH3 also inhibited EC cell invasion and migration in vitro and in vivo by regulating the epithelial-mesenchymal transition (EMT). Conversely, GOLPH3 overexpression promoted proliferation and migration. CONCLUSIONS: The present study provides evidence that GOLPH3 promotes EMT and metastasis of EC cells and predicts the risk of EC progression, highlighting its potential as a therapeutic target for this malignancy.
