The Role of PRMT7 and KLF4 in Driving the Malignant Progression of Gastric Cancer

Abstract

This study investigates the impact of PRMT7 on the malignant behaviors of gastric cancer (GC) and explores its potential as a therapeutic target for GC treatment. Clinical specimens and cytological experiments were analyzed to assess the effects of PRMT7. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to measure relative levels of PRMT7 in 48 pairs of GC and adjacent normal tissues. The influence of PRMT7 on clinical features and prognosis in GC patients was examined. The regulatory effects of PRMT7 on proliferative and migratory potentials in GC cells were evaluated using cell counting kit-8 (CCK-8) and transwell assay, respectively. Additionally, the role of PRMT7 and its downstream target in regulating malignant behaviors of GC was elucidated. Results showed that PRMT7 was upregulated in GC tissues, and its high expression in GC patients was associated with tumor staging and lymphatic metastasis, indicating a poor prognosis. PRMT7 stimulated proliferative and migratory potentials in GC cells, and KLF4 was identified as the downstream gene of PRMT7 responsible for the PRMT7-mediated malignant phenotypes of GC. In conclusion, PRMT7 is upregulated in GC tissues and its elevated levels are closely linked to tumor staging and lymphatic metastasis, predicting an unfavorable prognosis. PRMT7 drives the proliferative and migratory potentials of GC cells through the negative regulation of KLF4. The findings suggest that PRMT7 could be a potential therapeutic target for GC.