Long non‑coding RNA‑ZNF281 promotes cancer cell migration and invasion in gastric cancer via downregulation of microRNA‑124
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- Published online on: January 10, 2020 https://doi.org/10.3892/ol.2020.11286
- Pages: 1849-1855
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Copyright: © Gao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
It has previously been determined that long non‑coding (lnc)RNA‑zinc finger protein (ZNF)281 serves an oncogenic role in breast cancer; however, the role of lncRNA‑ZNF281 in other cancer types is yet to be elucidated. The present study aimed to analyze the role of ZNF281 in gastric cancer by characterizing its activity in cancerous tissues and normal tissues using RT‑qPCR. Overexpression experiments were also performed to investigate the interaction between ZNF281 and miR‑124, and Transwell assays were conducted to analyze cell invasion and migration. The present study revealed that lncRNA‑ZNF281 was upregulated, and that microRNA (miR)‑124 was downregulated, in cancerous tissues compared with that in the paired adjacent healthy tissues of patients with gastric cancer. In addition, the expression levels of lncRNA‑ZNF281 and miR‑124 exhibited a significant inverse association. Furthermore, in vitro cell experiments determined that lncRNA‑ZNF281 overexpression resulted in miR‑124 inhibition, yet miR‑124 overexpression did not influence lncRNA‑ZNF281 expression. lncRNA‑ZNF281 expression level was also associated with the clinical stage of the patient. Bioinformatics analysis revealed that lncRNA‑ZNF281 may target the base pairs in the hairpin loop of the miR‑124 precursor. Subsequent in vitro cell experiments indicated that lncRNA‑ZNF281 overexpression resulted in promoting the migration and invasiveness of gastric cancer cells, while miR‑124 over‑expression led to its inhibition. In addition, miR‑124 overexpression partially recovered the effects of lncRNA‑ZNF281 overexpression. Therefore, lncRNA‑ZNF281 may promote cancer cell migration and invasion in gastric cancer via downregulation of miR‑124.
