Abstract: Background and Objective: Gastric Carcinoma (GC) is categorized among malignant tumours with an extremely increased fatality rate, with an incidence constantly rising in recent years. Accumulating studies have pointed out that lncRNA may be the breakthrough in the fight against tumour diseases. The purpose of this investigation was to explore the mechanism of lncRNA PVT1 on gastric carcinoma cells. Materials and Methods: SGC7901 and MGC803 GC cell multiplication, invasion and apoptosis were studied under altering expressions of PVT1 and miR-423-5p. The interaction between both was further confirmed by the Dual-Luciferase Reporter Assay (DLRA). Results: Silencing PVT1 and increasing miR-423-5p hampered GC cell multiplication and invasiveness capacity and enhanced apoptosis while overexpression had opposite effects (p<0.05). The online target gene prediction website identified a reciprocal binding locus between PVT1 and miR-423-5p and DLRA confirmed the targeting relationship (p<0.05). After inhibiting PVT1, miR-423-5p in GC cells increased (p<0.05). Moreover, the salvage experiment demonstrated that reduced expression levels of PVT1 on GC cells were restored by simultaneously inhibiting miR-423-5p (p>0.05). Conclusion: PVT1 participates in gastric carcinogenesis and progression through the targeted inhibition of miR-423-5p to promote cell activity and reduce apoptosis, which may be a breakthrough in GC research regarding its diagnosis and treatment.