Effects of FAM172A protein on HepG2 cell proliferation and related signaling pathways / 中华肝胆外科杂志

ABSTRACT

Objective To analyze the effect of FAM172A protein on HepG2 cell proliferation and related signaling pathways,and provide a theoretical basis for the new target of liver cancer treatment.Methods The liver tissue was removed from March 2016 to February 2018 in the Air Force Characteristic Medical Center (formerly the People's Liberation Army Air Force General Hospital).The liver tissues were surgically resected,including normal liver tissue and liver infected with hepatitis B virus (HBV) tissue and liver cancer tissue,HepG2 cells were randomly divided into experimental group and control group.The experimental group was co-transfected with FAM172A protein granules and fluorescent protein-labeled plasmids,and the control group was left without any treatment.The position of FAM172A protein in HepG2 cells was observed by laser confocal microscopy.The content of FAM172A in LO2,HepG2 and HerpG2.2.15 cells was determined.Different concentrations of FAM172A recombinant protein solution were co-incubated with HepG2 cells for different time.Cell cycle and cell count were detected by flow cytometry,and Notch signal and cyclin expression were detected by Western blot.Results The FAM172A protein was located in the endoplasmic reticulum of HepG2 cells and was clearly expressed in normal liver tissues,and was decreased in liver tissues of patients with HBV infection.With the increase of the concentration of FAM172A,the inhibitory effect on the proliferation of hepatoma cells was more obvious,and it was concentration-dependent.After HepG2 cells were treated with 100 pg/L FAM172A for 48 hours,the percentage in the S phase decreased to 2.27％ and in the G1 phase increased to 77.49％,the cell cycle was completely blocked in the G1/S phase.Electrophoresis results showed that only the relative expression of Notch3 protein and cyclin E increased.Conclusion FAM172A may be a novel tumor suppressor gene that inhibits the proliferation of hepatoma cells by activating Notch3 signaling pathway and up-regulating the expression of cyclin E.