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Objective   This study is aimed at exploring the regulatory mechanism of 73HOXC-AS1 overexpression plasmid-activated Wnt β -catenin classic signaling pathway and eukaryotic initiation factor 4A (eIF4AIII) expression increased by lentivirus-eIF4AIII-RNAi (44682-1) (LV-eIF4AIII-RNAi (44682-1)).Methods   Focusing on the occurrence and progression of gastric cancer, the human gastric cancer cell line BGC823 (University Experimental Center) was taken as the research object and was transfected after subculture. According to the different ways of transfection, the cells were divided into the P1 group (LV-eIF4AIII-RNAi (44682-1) overexpressed plasmid), the P2 group (pcDNA-HOXC-AS1 overexpressed plasmid), the P3 group (LV-eIF4AIII-RNAi (44682-1) + pcDNA-HOXC-AS1), and the P4 group (no transfection, control group). Cell proliferation was detected by CCK-8 (Cell Counting Kit-8) assay, Western blotting was adopted to detect Wnt3a and P-GSK3 β  proteins, Transwell assay was adopted to detect the ability of cell migration and invasion, and cell cycle and apoptosis were detected by flow cytometry.Results   The results show that the protein expression levels of Wnt3a and P-GSK3 β  (glycogen synthase kinase-3 β ) in the P1 and P4 groups were lower than those in the P2 and P3 groups ( P  < 0.05). The cell activity and clone number of BGC823 in the P3 group were higher than those in the P1, P2, and P4 groups ( P  < 0.05). The apoptosis rate of BGC823 cells in the P3 group was significantly higher than those in the P1, P2, and P4 groups ( P  < 0.05). The proportion of BGC823 cells in the P3 group at the S phase was significantly higher than those in the P1, P2, and P4 groups, while the proportion in the G2 phase was significantly lower than those in the P1, P2, and P4 groups ( P  < 0.05). The number of migrating and invading BGC823 cells in the P3 group was significantly higher than those in the P1, P2, and P4 groups, while the number of migrating BGC823 cells in the P4 group was significantly lower than those in the P1 and P2 groups ( P  < 0.05).Conclusion   The 73HOXC-AS1 overexpression plasmid-activated Wnt β -catenin classic signaling pathway and eIF4AIII expression increased by LV-eIF4AIII-RNAi (44682-1) could act together on BGC823 cells to improve cell proliferation activity, migration, and invasion; inhibit cell apoptosis; and prevent cells from entering the S phase.

Molecular Mechanism of 73HOXC-AS1-Activated Wntβ-Catenin Signaling and eIF4AIII in Promoting Progression of Gastric Cancer