Function and mechanism exploration of zinc finger protein 64 in lung adenocarcinoma cell growth and metastasis

This paper aims to discover the effect of Zinc Finger Protein 64 (ZFP64) and Notch pathway on lung adenocarcinoma cell. ZFP64 expression in Cancer tissue and overall survival analysis was identified by TCGA-LUAD. ZFP64 expressions in tumor tissue (n = 30) and adjacent tissue (n = 30), and in human nontumorigenic bronchial epithelial cell line BEAS-2B and human lung adenocarcinoma cell lines (H23, H1975, H2228, and H2085) were measured via quantitative real-time polymerase chain reaction (qRT-PCR). H1975 cell viability, cell cycle progression, and migration after transfection or under Notch Inhibitor MK-0752 treatment were detected through MTT assay, flow cytometer, and wound healing assay, respectively. Expressions of Notch intracellular domain (NICD) and hairy and enhancer of split 1 (Hes-1) in H1975 cell were determined by western blot. Epithelial-mesenchymal transition (EMT)-related proteins (E-Cadherin and Vimentin) expressions were identified through qRT-PCR and western blot. ZFP64 expression in lung adenocarcinoma tissue and lung adenocarcinoma cell lines was higher and related to poor prognosis. After transfection, H1975 cell viability, migration, and expressions of Vimentin, NICD and Hes-1 were upregulated yet cell percentage in G0/G1 phase, E-cadherin expression was downregulated by overexpressed ZFP64. However, Notch Inhibitor MK-0752 inhibited the effects of overexpressed ZFP64 on H1975 cell viability, cell cycle, migration, EMT progress, and Notch pathway activation. Overexpressed ZFP64 promoted the development of lung adenocarcinoma cells by activating Notch pathway.