G-F Wang1, L-N Wen. 1. Department of Radiotherapy, Department of Obstetrics and Gynecology; Liaocheng People's Hospital, Liaocheng, China. 2015020671@stu.sdnu.edu.cn.
Abstract
OBJECTIVE: Previous studies have shown that long non-coding RNA (lncRNA) SNHG14 can act as a cancer-promoting gene, but the role of SNHG14 in the development of endometrial carcinoma (EC) has not been reported. This study was designed to investigate the expression characteristics of SNHG14 in EC tissues and cells and to specify whether SNHG14 promotes the malignant progression of EC by modulating microRNA-655-3P. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qPCR) was carried out to examine SNHG14 expression in tumor tissue specimens and paracancerous tissue specimens collected from 52 patients with EC, and the relationship between SNHG14 expression and clinical indicators or prognosis of these subjects was analyzed as well. Further, the expression level of SNHG14 in EC cell lines was also verified by qRT-PCR. In addition, SNHG14 knockdown and the overexpression models were constructed using lentivirus in EC cell lines, Ishikawa, and KLE, and the influence of SNHG14 on EC cell biological functions was evaluated by Cell Counting Kit-8 (CCK-8), plate cloning, 5-ethynyl-2'-deoxyuridine (EdU) and flow apoptosis assays. Finally, in vitro recovery experiments were conducted to explore the mechanism by which SNHG14 interacts with microRNA-655-3P to exert its effect on the progression of EC. RESULTS: qPCR results indicated that SHHG14 expression in EC tumor tissues was remarkably higher than that in adjacent tissues. Compared with patients with low expression of SNHG14, patients with high expression of SNHG14 had larger tumor size, lower overall survival, and more advanced pathological stage. In vitro, compared with those in the control group, the overexpression of SNHG14 markedly enhanced EC cell proliferation while inhibited cell apoptosis, and the opposite result was observed in SNHG14 silencing group. Subsequently, qRT-PCR verified that microRNA-655-3P expression was significantly reduced in EC tissues and negatively correlated with SNHG14. In addition, recovery experiment revealed a mutual regulation between SNHG14 and microRNA-655-3P, the two of which may together modulate the malignant progression of EC. CONCLUSIONS: EC tumor tissues contain a significantly high expression of LncRNA SNHG14, which has been confirmed to be remarkably associated with tumor size, pathological stage, and poor prognosis of EC patients. Additionally, lncRNA SNHG14 is capable of accelerating malignant progression of EC by regulating microRNA-655-3P expression.
OBJECTIVE: Previous studies have shown that long non-coding RNA (lncRNA) SNHG14 can act as a cancer-promoting gene, but the role of SNHG14 in the development of endometrial carcinoma (EC) has not been reported. This study was designed to investigate the expression characteristics of SNHG14 in EC tissues and cells and to specify whether SNHG14 promotes the malignant progression of EC by modulating microRNA-655-3P. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qPCR) was carried out to examine SNHG14 expression in tumor tissue specimens and paracancerous tissue specimens collected from 52 patients with EC, and the relationship between SNHG14 expression and clinical indicators or prognosis of these subjects was analyzed as well. Further, the expression level of SNHG14 in EC cell lines was also verified by qRT-PCR. In addition, SNHG14 knockdown and the overexpression models were constructed using lentivirus in EC cell lines, Ishikawa, and KLE, and the influence of SNHG14 on EC cell biological functions was evaluated by Cell Counting Kit-8 (CCK-8), plate cloning, 5-ethynyl-2'-deoxyuridine (EdU) and flow apoptosis assays. Finally, in vitro recovery experiments were conducted to explore the mechanism by which SNHG14 interacts with microRNA-655-3P to exert its effect on the progression of EC. RESULTS: qPCR results indicated that SHHG14 expression in EC tumor tissues was remarkably higher than that in adjacent tissues. Compared with patients with low expression of SNHG14, patients with high expression of SNHG14 had larger tumor size, lower overall survival, and more advanced pathological stage. In vitro, compared with those in the control group, the overexpression of SNHG14 markedly enhanced EC cell proliferation while inhibited cell apoptosis, and the opposite result was observed in SNHG14 silencing group. Subsequently, qRT-PCR verified that microRNA-655-3P expression was significantly reduced in EC tissues and negatively correlated with SNHG14. In addition, recovery experiment revealed a mutual regulation between SNHG14 and microRNA-655-3P, the two of which may together modulate the malignant progression of EC. CONCLUSIONS:EC tumor tissues contain a significantly high expression of LncRNA SNHG14, which has been confirmed to be remarkably associated with tumor size, pathological stage, and poor prognosis of EC patients. Additionally, lncRNA SNHG14 is capable of accelerating malignant progression of EC by regulating microRNA-655-3P expression.