ATF1 promotes the malignancy of lung adenocarcinoma cells by transcriptionally regulating ZNF143 expression

Abstract

The clinical oncogenic functions and mechanisms of activating transcription factor 1 (ATF1) in the progression of lung adenocarcinoma have not been completely elucidated. In this study, by employing human lung adenocarcinoma tissues and cells, we detect the correlation of ATF1 expression with the clinicopathological features and prognosis of patients with lung adenocarcinoma and find that ATF1 promotes lung adenocarcinoma cell proliferation and migration by transcriptionally enhancing zinc finger protein 143 (ZNF143) expression. ATF1 and ZNF143 are strongly expressed in lung adenocarcinoma tissues compared with those in the adjacent normal tissues, and high ATF1 and ZNF143 expressions are related to poor disease-free survival of lung adenocarcinoma patients. ATF1 overexpression results in increased proliferation and migration of lung adenocarcinoma cells, whereas knockdown of ATF1 inhibits cell proliferation and migration. Furthermore, ATF1 transcriptionally regulates the expression of ZNF143, and ATF1 and ZNF143 expressions are positively correlated in lung adenocarcinoma tissues. ZNF143 knockdown blocks lung adenocarcinoma cell migration, which is mediated by ATF1 upregulation. Hence, this study provides a potential therapeutic candidate for the treatment of lung adenocarcinoma.

Promotion of stem cell-like phenotype of lung adenocarcinoma by FAM83A via stabilization of ErbB2

“…Lung cancer ranks second among frequently diagnosed neoplastic disorders, surpassed only by breast cancer, yet it bears the highest mortality rates, contributing to 18% of total cancer deaths [ 1 , 2 ]. Lung adenocarcinoma (LUAD), a subtype of non-small cell lung cancer (NSCLC), accounts for around 40% of all lung cancers [ 3 – 5 ]. A majority of patients may have metastases or be in an advanced state when diagnosed, limiting therapeutic options and resulting in a poor prognosis [ 6 ].…”