Abstract

In recent decades, most gastric cancer patients are diagnosed in the advanced disease stage with poor prognosis, and more than half of the advanced-stage patients will relapse. This research explores lncRNA ZEB1-AS1’s effect on gastric cancer cell proliferation, invasion, apoptosis via regulating the miR-200b/Wnt1 molecular axis. ZEB1-AS1 and miR-200b expressions in BGC-803, SGC-7901, MKN-45, and AGS cells were measured by qRT-PCR. ZEB1-AS1 siRNA, miR-200b mimics, and miR-200b mimics + pcDNA3.1-ZEB1-AS1 were transfected into BGC-803 cells to study their respective effect on cell proliferation, invasion, apoptosis using CCK-8 and Transwell assays and flow cytometry, respectively. Dual-luciferase reporter gene assay is used to detect the luciferase activity of ZEB1-AS1 WT or MUT and Wnt1 WT or MUT after co-transfecting with miR-200b mimics. The expression of miR-200b in BGC-803 cells with knocked down or overexpressed ZEB1-AS1 was quantified with qRT-PCR. Western blot analysis was used to detect the protein level of Wnt1 in BGC-803 cells with upregulated or downregulated miR-200b expression. Data showed that ZEB1-AS1 expression was significantly raised when miR-200b expression was reduced (P < 0.05). BGC-803 cells were selected for follow-up experiments. ZEB1-AS1, Wnt1, and miR-200b were found to have a targeted regulatory relationship. The knockdown of ZEB1-AS1 and upregulation of miR-200b can hinder BGC-803 cell proliferation and invasion and expedite apoptosis. ZEB1-AS1 and miR-200b overexpression can reverse the effect of miR-200b upregulation on BGC-803 cell proliferation, invasion, and apoptosis. Therefore, lncRNA ZEB1-AS1 could impede gastric cancer cell proliferation and invasion and accelerate apoptosis via the regulation of the miR-200b/Wnt1 molecular axis.

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