SNHG10 Promotes Cell Proliferation and Migration in Gastric Cancer by Targeting miR-495-3p/CTNNB1 Axis
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ORIGINAL ARTICLE
SNHG10 Promotes Cell Proliferation and Migration in Gastric Cancer by Targeting miR‑495‑3p/CTNNB1 Axis Xiu Yuan1 · Tianwen Yang1 · Yun Xu1 · Shan Ou1 · Peng Shi1 · Ming Cao1 · Xin Zuo1 · Qinglan Liu1 · Jie Yao1 Received: 25 November 2019 / Accepted: 21 August 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Background Long non-coding RNAs have been acknowledged as the crucial regulators in the progression of human cancers, including gastric cancer (GC). Small nucleolar RNA host gene 10 (SNHG10) has been identified as an oncogene in several cancer types. Nonetheless, it is unclear whether SNHG10 exerts functions in GC cells. Aims The aims of the current study were to explore the function and underlying mechanism of SNHG10 in GC. Methods The expression levels of SNHG10, miR-495-3p and catenin beta 1 (CTNNB1) were detected by RT-qPCR. Lossof-function assays, including CCK-8, colony formation assay, flow cytometry analysis and transwell assays, were conducted to verify the effect of SHNG10 on the proliferation, apoptosis, migration and invasion of GC cells. Mechanism experiments were performed to identify the downstream molecular mechanism of SNHG10. Results SNHG10 was expressed at a high level in GC cells. Knockdown of SNHG10 inhibited the proliferation, migration and invasion of GC cells. Silencing of SNHG10 led to the downregulation of core factors of WNT signaling pathway. Knockdown of SNHG10 could decline the expression of CTNNB1 through sequestering miR-495-3p. Conclusions SNHG10 promotes the procession of GC through targeting miR-495-3p/CTNNB1 and activating WNT signaling pathway. Keywords SNHG10 · miR-495-3p · CTNNB1 · Gastric cancer
Introduction Gastric cancer (GC) is one of commonest digestive tract tumors [1]. Accumulating researches indicated that dietary factors are the major causes leading to pathology of GC [2]. Chemotherapy and surgical excision are the usual methods using to treat GC [3, 4]. The recurrence rate is increasing due to the high metastasis. Thus, it is necessary to investigate the molecular mechanism associated with the GC progression. Long non-coding RNAs (lncRNAs) are vital regulators in the multiple cancers [5]. Recent years, more and more Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10620-020-06576-w) contains supplementary material, which is available to authorized users. * Jie Yao [email protected] 1
Department of Gastroenterology, The Sixth People’s Hospital of Chongqing, Chongqing 400000, China
lncRNAs have been reported as biological participants in GC. For example, ANRIL accelerates the drug resistance in GC cells [6]. UCA1 enhances multidrug resistance in GC [7]. LncRNA CRNDE acts as a tumor promoter in GC [8]. LncRNA-PVT1 facilitates the growth and invasion of gastric cancer by interacting with FOXM1 [9]. Small nucleolar RNA host gene 10 (SNHG10) has been verified to be a tumor promoter in hepatocellular carcinoma [10], bladder cancer [11], and non-small cell lung
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