NEIL3 contributes toward the carcinogenesis of liver cancer and regulates PI3K/Akt/mTOR signaling

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. NEIL3 promotes progression and predicts survival in cancer. However, its role in liver cancer remains unclear. Based on data in the TCGA database, NEIL3 exhibited much higher expression in liver cancer tissues and was clinically correlated with tumor grade in patients with liver cancer. Furthermore, high NEIL3 expression caused shorter survival times. In liver cancer cell lines, NEIL3 showed abundant expression. When NEIL3 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 NEIL3-overexpression but decreased following NEIL3-knockdown. In conclusion, NEIL3 contributes toward development and/or progression in liver cancer and regulates PI3K/Akt/mTOR signaling.

Automated summary

In liver cancer, high NEIL3 expression is associated with tumor grade and survival time. NEIL3 is abundantly expressed in liver cancer cell lines, and its knockdown impairs cell functions, causes cell cycle arrest at G2 phase, and increases apoptotic rate. Additionally, NEIL3 regulates the PI3K/Akt/mTOR signaling pathway in liver cancer.