Huimin Guo1, Shenghua Yang2, Shaoru Li2, Mengting Yan2, Li Li2, Hongxia Zhang3. 1. Department of Gynecology, The First Affiliated Hospital of Xinxiang Medical University Weihui, Henan, 453100, PR China. Electronic address: huimin0723@163.com. 2. Department of Gynecology, The First Affiliated Hospital of Xinxiang Medical University Weihui, Henan, 453100, PR China. 3. Department of Obstetrics and Gynecology, Huaihe Hospital of Henan University, Kaifeng, Henan, 475000, PR China.
Abstract
BACKGROUND: Recent studies highlight the crucial regulatory roles of long non-coding RNAs (lncRNAs) in carcinogenesis. However, involvement of the lncRNA SNHG20 in cervical cancer progression remains unclear. METHODS: The expression of SNHG20 and miR-140-5p was determined in cervical cancer. Gain or loss of function assays were used to explore the roles of SNHG20 and miR-140-5p in cervical cancer cells. Luciferase assay and Western blot were used to explore the underlying mechanisms of SNHG20 and miR-140-5p in cervical cancer progression. RESULTS: QRT-PCR showed that SNHG20 expression was significantly increased in cervical cancer. MiR-140-5p acted as a downstream target of SNHG20. SNHG20 inhibition or miR-140-5p overexpression reduced cervical cancer cells proliferation and invasion ability. Furthermore, we identified that ADAM10 could act as a potential target of miR-140-5p. MEK/ERK signaling could be inhibited by miR-140-5p mimics in cervical cancer cells. In addition, ADAM10 overexpression abrogated the effect of miR-140-5p mimics on cervical cancer cells proliferation and invasion. CONCLUSIONS: Our study demonstrated that SNHG20 could function as an oncogenic lncRNA by regulating miR-140-5p-ADAM10 axis and MEK/ERK signaling pathway in cervical cancer.
BACKGROUND: Recent studies highlight the crucial regulatory roles of long non-coding RNAs (lncRNAs) in carcinogenesis. However, involvement of the lncRNA SNHG20 in cervical cancer progression remains unclear. METHODS: The expression of SNHG20 and miR-140-5p was determined in cervical cancer. Gain or loss of function assays were used to explore the roles of SNHG20 and miR-140-5p in cervical cancer cells. Luciferase assay and Western blot were used to explore the underlying mechanisms of SNHG20 and miR-140-5p in cervical cancer progression. RESULTS: QRT-PCR showed that SNHG20 expression was significantly increased in cervical cancer. MiR-140-5p acted as a downstream target of SNHG20. SNHG20 inhibition or miR-140-5p overexpression reduced cervical cancer cells proliferation and invasion ability. Furthermore, we identified that ADAM10 could act as a potential target of miR-140-5p. MEK/ERK signaling could be inhibited by miR-140-5p mimics in cervical cancer cells. In addition, ADAM10 overexpression abrogated the effect of miR-140-5p mimics on cervical cancer cells proliferation and invasion. CONCLUSIONS: Our study demonstrated that SNHG20 could function as an oncogenic lncRNA by regulating miR-140-5p-ADAM10 axis and MEK/ERK signaling pathway in cervical cancer.