Abstract
Gastric cancer (GC) remains a serious disease to human health with high mortality worldwide. Evolving evidence implied that long non-coding RNA Opa interacting protein 5-antisense RNA1 (OIP5-AS1) went in for the pathological progress of GC. Nevertheless, the potential molecular mechanism of OIP5-AS1 needed to be further investigated. Levels of OIP5-AS1, microRNA (miR)-153-3p, and zinc finger and BTB domain containing 2 (ZBTB2) were assessed using quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot assays. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) was implemented to detect cell proliferation in vitro. Cell apoptosis was evaluated by flow cytometry. Besides, transwell assay was conducted to examine cell migration and invasion in AGS and MKN45 cells. The interaction between miR-153-3p and OIP5-AS1 or ZBTB2 was validated utilizing dual-luciferase reporter assay. Lastly, the role of OIP5-AS1 in tumor growth was researched through adopting xenograft tumor model. OIP5-AS1 and ZBTB2 were strongly higher in GC tissues than noncancerous samples. OIP5-AS1 silencing remarkably curbed cell proliferation, migration and invasion, and elevated cell apoptosis in both AGS and MKN45 cells. Functional analysis indicated that OIP5-AS1 regulated ZBTB2 expression via binding to miR-153-3p. Moreover, the role of miR-153-3p in cell growth and metastasis was abrogated by ZBTB2 overexpression. Above all, OIP5-AS1 could reduce the growth of xenograft tumor in vivo. OIP5-AS1 exerted its role via miR-153-3p/ZBTB2 axis in the progression of GC cells. These findings might supply a biomarker for the diagnosis and therapy of GC clinically.
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