H-H Chen1, J Zong, S-J Wang. 1. Department of Neurosurgery, The First People's Hospital of Wenling, Wenling, Zhejiang, China. wshh446771@163.com.
Abstract
OBJECTIVE: Recent evidence shows that gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC) acts as a critical role in the proliferation and metastasis in several tumors. We aimed to explore the expression pattern, function, and potential mechanism of GAPLINC in glioblastoma multiforme (GBM). PATIENTS AND METHODS: The expression levels of GAPLINC and its clinical significance were determined by analyzing TCGA datasets. RT-PCR was performed to detect the levels of GAPLINC and miR-331-3p. CCK-8, colony formation, EdU assays, wound healing assay and transwell invasion assay were performed to analyze the effect of GAPLINC on GBM behaviors. MiRNAs that may interact with GAPLINC were predicted using StarBase and RegRNA 2.0. A luciferase reporter assay was used to detect the targeting effect of GAPLINC on miR-331-3p. RESULTS: We found that GAPLINC expression was significantly up-regulated in both GBM tissues and cell lines. The overexpression of GAPLINC was associated with shorter overall survival and disease-free survival. Functional assays indicated that GAPLINC silencing suppressed GBM cells proliferation, migration, and invasion, and promoted apoptosis. In the mechanism, we found that GAPLINC acted as a competing endogenous RNA to sponge miR-331-3p and knockdown of GAPLINC promoted the expression of miR-331-3p. CONCLUSIONS: Our findings suggested that GAPLINC served as an oncogenic lncRNA in GBM through negative modulation of miR-331-3p, providing a novel treatment targeting for GBM.
OBJECTIVE: Recent evidence shows that gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC) acts as a critical role in the proliferation and metastasis in several tumors. We aimed to explore the expression pattern, function, and potential mechanism of GAPLINC in glioblastoma multiforme (GBM). PATIENTS AND METHODS: The expression levels of GAPLINC and its clinical significance were determined by analyzing TCGA datasets. RT-PCR was performed to detect the levels of GAPLINC and miR-331-3p. CCK-8, colony formation, EdU assays, wound healing assay and transwell invasion assay were performed to analyze the effect of GAPLINC on GBM behaviors. MiRNAs that may interact with GAPLINC were predicted using StarBase and RegRNA 2.0. A luciferase reporter assay was used to detect the targeting effect of GAPLINC on miR-331-3p. RESULTS: We found that GAPLINC expression was significantly up-regulated in both GBM tissues and cell lines. The overexpression of GAPLINC was associated with shorter overall survival and disease-free survival. Functional assays indicated that GAPLINC silencing suppressed GBM cells proliferation, migration, and invasion, and promoted apoptosis. In the mechanism, we found that GAPLINC acted as a competing endogenous RNA to sponge miR-331-3p and knockdown of GAPLINC promoted the expression of miR-331-3p. CONCLUSIONS: Our findings suggested that GAPLINC served as an oncogenic lncRNA in GBM through negative modulation of miR-331-3p, providing a novel treatment targeting for GBM.