[No authors listed]
OBJECTIVE:Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators of various tumors. Currently, lncRNA OPI5-AS1 (OPI5-AS1) has been identified as a tumor suppressor gene involved in several cancers. Therefore, the aim of this study was to investigate the function of OPI5-AS1 in gastric cancer (GC) progression. PATIENTS AND METHODS:Quantitative Real (qRT-PCR) was used to detect the expressions of OPI5-AS1 and microRNA-641 (miR-641) in tissues and cells. The Cell Counting Kit-8 (CCK-8), colony formation, and 5-Ethynyl-2'-deoxyuridine (EDU) assays were used to verify the effect of OPI5-AS1 on cell proliferation. Cell cycle distribution was detected by flow cytometry. Furthermore, Western blot was performed to detect the protein expressions of cyclin D1 and p-AKT. RESULTS:OPI5-AS1 was significantly upregulated, while miR-641 was downregulated in GC tissues and cells. OPI5-AS1 expression was remarkably inversely correlated with miR-641 in GC. Moreover, OPI5-AS1 could sponge miR-641 and regulate its expression in GC cells. Functional experiments showed that OPI5-AS1 overexpression remarkably accelerated GC cell proliferation and cell cycle. However, miR-641 overexpression could reverse the functional effects induced by OPI5-AS1 overexpression. CONCLUSIONS:OPI5-AS1 overexpression promotes tumorigenesis and development of GC by sponging miR-106a-5p. In addition, our findings suggest that OPI5-AS1 may serve as an innovative and prospective therapeutic target for GC.
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