Aberrantly ASF1B Promotes Proliferation and Metastasis of Lung Adenocarcinoma in Vitro Study

Abstract

ASF1A and ASF1B are two isoforms of the histone H3–H4 chaperone anti-silencing feature 1 (ASF1) found in mammalian cells. To date, however, it remains elusive if they have different physiological functions in lung adenocarcinoma. Here, we identified both ASF1A and ASF1B are elevated in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). ASF1B, but not ASF1A is associated with poor clinical outcomes and act as an independent prognostic factor in LUAD. In vitro studies, knockdown of ASF1B inhibits the proliferation of lung adenocarcinoma through modulating the expression of cyclins and CDK inhibitor (CKI). Moreover, by restraining epithelial-mesenchymal transition (EMT), abnormal of ASF1B could limit metastasis of lung adenocarcinoma. In summary, ASF1B is important in the development of NSCLC and can provide a novel target for lung cancer therapy.