CHD4 Inhibits Lung Adenocarcinoma Cell Apoptosis and Induces Proliferation via Upregulating PHF6

Abstract

Aim: The crucial impacts of chromodomain helicase DNA binding protein 4 (CHD4) upon repressing apoptosis and programmed cell death and promoting cancer development have been widely reported. To further complement the findings, this study investigates the apoptosis-modulating role of CHD4 in lung adenocarcinoma (LAC). Methods: Quantitative reverse transcription polymerase chain reaction was used to detect the expression of CHD4 and plant homeodomain finger protein 6 (PHF6) in lung cancer tissues and LAC cells. After LAC cells (A549 and Calu-3) transfected with small interfering RNA for PHF6 (si-PHF6) or CHD4 overexpression plasmid, the apoptosis, cell cycle transition and colony formation were examined through functional analyses including flow cytometry and colony formation assays. Results: CHD4 and PHF6 expressions were higher in lung cancer tissues than in matched adjacent normal tissues (p < 0.001). Silencing of PHF6 in LAC cells enhanced LAC cell apoptosis and inhibited cell cycle transition and proliferation (p < 0.001). The overexpression of CHD4 increased the PHF6 level and reversed the impact of PHF6 silencing in LAC cells (p < 0.001). Conclusions: CHD4 promotes the proliferation of LAC cells and suppresses their apoptosis by elevating the levels of PHF6.