Neoplasma. 2020 Feb 17;:
Authors: Zhang W, Zhan F, Li D, Wang T, Huang H
Abstract
Gastric cancer (GC), one of the most common cancers worldwide, presents a considerable threat to human health. Although multiple investigations have been made to figure out therapies for this disease, the prognosis of patients suffered with GC remains poor. It has been reported that lncRNAs exerted their significant effects on numerous cancers. Evidences confirmed that lncRNA RGMB-AS1 played an oncogenic role in the progression of cancers. However, the biological function and molecular mechanism of RGMB-AS1 in GC haven't been explored. In this study, our results demonstrated that RGMB-AS1 was upregulated in GC cells and knockdown of RGMB-AS1 suppressed cell proliferation, migration, invasion, EMT process and promoted cell apoptosis. Molecular mechanism experiments indicated that RGMB-AS1 could bind with miR-22-3p and NFIB was a downstream target gene of miR-22-3p. Additionally, RGMB-AS1 suppression up-regulated the expression of miR-22-3p and miR-22-3p inhibitor could reverse the inhibitive role of sh-RGMB-AS1-1 in NFIB expression. Rescues assays showed that NFIB overexpression partially recovered the inhibitory function on cell proliferation, migration, invasion, EMT process and the promotive function on cell apoptosis caused by RGMB-AS1 depletion. Taken together, RGMB-AS1 contributes to the progression of GC by regulating miR-22-3p/NFIB axis, indicating a new therapeutic target for GC treatment.
PMID: 32064882 [PubMed - as supplied by publisher]
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου