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Published:
Jun 6, 2023DOI:
10.4314/tjpr.v22i5.3Keywords:
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Main Article Content
E2F6 promotes cell proliferation and invasion in gastric cancer through the regulation of lncRNA TUSC7
Abstract
Purpose: To examine the regulatory effects of E2F6/long noncoding ribonucleic acid (lncRNA) TUSC7 on the progression of gastric cancer (GC), and the underlying mechanism of action.
Methods: Relative levels of E2F6 and TUSC7 in GC tissues were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The influence of TUSC7 on the overall survival of patients with GC was analyzed using Kaplan-Meier method. Interaction between E2F6 and TUSC7 was analyzed by Spearman correlation test and dual-luciferase reporter gene assay. Changes in proliferation, invasion and apoptosis of BGC823 and SGC7901 cells regulated by E2F6 and TUSC7 were assessed. The protein levels of MMP-2 and the activity of caspase-3 were evaluated in GC cells treated with E2F6 and TUSC7 using western blot and caspase-3 kit.
Results: TUSC7 was downregulated while E2F6 was upregulated in GC tissues and cells. A negative correlation was observed between the expression levels of TUSC7 and E2F6, and a low level of TUSC7 predicted poor prognosis in GC patients. The knockdown of E2F6 attenuated cell viability and invasion, and stimulated the apoptosis of GC cells, but these were reversed by co-knockdown of TUSC7. In addition, knockdown of E2F6 downregulated MMP-2 protein levels, and upregulated caspase-3 GC cells, but these changes were partially reversed by co-transfection of si-TUSC7.
Conclusion: TSUC7 is downregulated in GC, and its low level predicts poor prognosis in GC patients. E2F6 promotes proliferation and invasion of GC cells by negatively regulating TUSC7. Therefore, E2F6/TUSC7 may be utilized as potential therapeutic targets for GC.
