Silencing of ZNF610 suppresses cell proliferation and migration in lung adenocarcinoma.

Zinc finger proteins (ZNFs) play a significant role in the initiation and progression of tumors. Nevertheless, the specific contribution of ZNF610 to lung adenocarcinoma (LUAD) remains poorly understood. This study sought is to elucidate the role of ZNF610 in LUAD. Transcript data of LUAD were obtained from The Cancer Genome Atlas Program (TCGA) database and processed via R program. The expression of ZNF610 was assessed in various cell lines. To compare the proliferative capacity of cells with or without ZNF610 silencing, CCK8, cell colony formation assay, and Celigo label‐free cell counting assay were employed. Furthermore, transwell migration and invasion assays were conducted to evaluate the migratory and invasive abilities of the cells. The expression levels of genes and proteins were assessed using quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blot techniques. In different LUAD cells, the expression level of ZNF610 was found to be significantly higher in LUAD cells compared to MRC‐5 and BASE‐2B cells. Moreover, the silencing of ZNF610 resulted in a decrease in cell proliferation and migration abilities. Additionally, the apoptosis rate of cells increased upon silencing ZNF610. Notably, the proportion of cells in the G0/G1 phase increased, while the proportion of cells in the S phase decreased following ZNF610 silencing. Finally, β‐catenin and snail were identified as downstream targets of ZNF610 in cells. Our findings suggest that silencing ZNF610 could inhibit LUAD cell proliferation and migration, possibly through the downregulation of β‐catenin and snail. Significance statement: Lung adenocarcinoma (LUAD) is an aggressive cancer, and elucidating novel therapeutic targets is crucial. Our study identified ZNF610 as a potential target by demonstrating its overexpression in LUAD cells and its functional role in cell proliferation, migration, and apoptosis. Silencing ZNF610 inhibited these processes and altered cell cycle distribution, suggesting its potential as a therapeutic target. Furthermore, we identified β‐catenin and snail as downstream targets of ZNF610, providing mechanistic insights into its oncogenic functions. These findings warrant further investigation of ZNF610 as a therapeutic target for LUAD. [ABSTRACT FROM AUTHOR]