ArticleAmerican journal of cancer research2025
ZNF710 regulates the proliferation, migration, apoptosis, and cell cycle progression of gastric cancer cells through the Wnt/β-catenin pathway.
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis study aimed to investigate the mechanism underlying the role of Zinc finger protein 710 (ZNF710) in gastric cancer (GC).
methodsThe level of ZNF710 expression in GC and its prognosis were examined based on the public databases and clinical samples. Cell models of lentivirus-mediated overexpression (oeZNF710) and knockdown (shZNF710) of ZNF710 were developed on the AGS and HGC-27 GC cell lines. The biological behaviors of these cells were analysed systematically, comprising proliferation (as measured by CCK-8 assay and plate cloning experiment), apoptosis (measured by flow cytometry), and migration (measured by Transwell assay). To confirm the expression of the main proteins of the Wnt/β-catenin system, western blotting analysis was conducted. Besides, functional rescue experiments of Wnt signaling agonist SKL2001 and Wnt signaling inhibitor XAV939 were performed. The in vivo activity of ZNF710 was tested in a nude mouse subcutaneous xenograft model.
resultsThe expression of ZNF710 was significantly increased in GC tissues and cell lines compared to standard controls, whereas high levels of ZNF710 were associated with a poor prognosis in GC patients. ZNF710 knockdown of HGC-27 cells significantly reduced cell proliferation, migration, and invasion and increased apoptosis. On the contrary, overexpression of ZNF710 in AGS cells produced the reverse effects. Mechanistically, ZNF710 overexpression increased the expression of Wnt/β-catenin pathway-related regulatory proteins, and ZNF710 knockdown reduced their expression.
conclusionZNF710 is highly expressed in GC and promotes GC cell proliferation, migration, and invasion while inhibiting apoptosis by activating the Wnt/β-catenin pathway, suggesting it may serve as a potential therapeutic target for GC.
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