The aim of this study was to characterize the involvement of long noncoding RNA HOTAIR in gastric cancer development. Measurement of HOTAIR and miRNA-206 expression by in situ hybridization (ISH) and analyzed for the correlation between HOTAIR and miRNA-206 in gastric cancer tissues. To evaluate the effects of HOTAIR in gastric cancer, MTT assay, flow cytometry, transwell, and wound healing assays were applied. To explain the mechanism behind HOTAIR's involvement, the expression of proteins related to it was also measured by Western blotting. Finally, correlations among related factors were determined by a luciferase target experiment. HOTAIR expression significantly increased, and miRNA-206 expression significantly decreased in cancer tissues (p < .01 and p < .001, respectively); HOTAIR knockdown suppressed cell viability, increased cell apoptosis by maintaining cells in the G1 phase, and inhibited cell invasion and migration by regulating miRNA-206 expression (p < .01 or p < .001). Meanwhile, with HOTAIR knockdown, CCND1 and CCND2 protein expressions were significantly suppressed, whereas miRNA-206 expression increased (p < .01 or p < .001). HOTAIR was shown to target miRNA-206 and miRNA-206 targeted CCND1 and CCND2. HOTAIR knockdown had antitumor effects by suppressing CCND1 and CCND2 expression by stimulating miRNA-206 in gastric cancer in vitro study.
Keywords: CCND1; CCND2; HOTAIR; gastric cancer; miRNA‐206.
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