Open AccessLong non-coding RNA OIP5-AS1 promotes cell proliferation and aerobic glycolysis in gastric cancer through sponging miR-186
Author(s) -
Jinxiong Huang,
ShuangShuang Hou,
Jian Xu,
Wu Ju,
Jun Yin
Publication year - 2019
Publication title -
archives of medical science/archives of medical science (online)
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 46
eISSN - 1896-9151
pISSN - 1734-1922
DOI - 10.5114/aoms.2019.87213
Subject(s) - gene knockdown , carcinogenesis , cell growth , oncogene , apoptosis , cancer research , cell culture , in vivo , competing endogenous rna , cell , biology , nude mouse , reporter gene , long non coding rna , downregulation and upregulation , microbiology and biotechnology , medicine , cancer , gene expression , cell cycle , biochemistry , gene , genetics
Long non-coding RNAs (lncRNAs) play vital roles in tumour initiation and progression. LncRNA OIP5-AS1 is a potential oncogene in many types of human malignancies, but its biological functions in gastric cancer (GC) remain to be further elucidated. Material and methods The expression levels of OIP5-AS1 and miR-186 in GC tissues and cell lines were detected by RT-qPCR analysis. CCK-8 assay and colony formation assay were performed to investigate the proliferation of GC cells in vitro, and a nude mouse tumour model was established to validate the role of OIP5-AS1 in GC tumorigenesis in vivo. The glucose consumption and lactate production of GC cells were detected by ELISA assay. Interaction between OIP5-AS1 and miR-186 was determined using dual luciferase reporter assay. Results The results demonstrated that OIP5-AS1 was upregulated in GC tissues and cell lines and that its high expression was notably correlated with aggressive clinicopathological features of GC patients. Functionally, knockdown of OIP5-AS1 inhibited GC cell proliferation and enhanced cell apoptosis in vitro, and inhibited GC xenograft growth in vivo. In addition, knockdown of OIP5-AS1 reduced the glucose consumption and lactate production in GC cells. In particular, OIP5-AS1 may function as a ceRNA for miR-186, and inhibition of miR-186 blocks the effects of OIP5-AS1 knockdown on aerobic glycolysis in GC cells. Conclusions Accordingly, our findings suggested that the OIP5-AS1/miR-186 axis might be considered as a potential therapeutic target for GC patients.