Abstract

Liver cancer is one of the top three fatal types of cancer and it causes several thousands of mortalities each year. The main treatment is surgical resection which shows little benefit for patients with recurrence or metastasis. <em>NEIL3</em> promotes progression and predicts survival in cancer. However, its role in liver cancer remains unclear. Based on data in the TCGA database, <em>NEIL3</em> exhibited much higher expression in liver cancer tissues and was clinically correlated with tumor grade in patients with liver cancer. Furthermore, high <em>NEIL3</em> expression caused shorter survival times. In liver cancer cell lines, <em>NEIL3</em> showed abundant expression. When <em>NEIL3</em> was knocked down in HepG2 and Huh‑7 cells, cell abilities including proliferation, growth, migration and invasion, exhibited deficiency to different extents. Cell cycle transition was blocked at the G2 phase and the cell apoptotic rate increased notably. In addition, the phosphorylation levels of Akt, PI3K and mTOR were increased following <em>NEIL3</em>‑overexpression but decreased following <em>NEIL3</em>‑knockdown. In conclusion, <em>NEIL3</em> contributes toward development and/or progression in liver cancer and regulates PI3K/Akt/mTOR signaling.