HBxAg suppresses apoptosis of human placental trophoblastic cell lines via activation of the PI3K/Akt pathway

The aim of this study is to investigate the effect of hepatitis B virus X (HBx) protein on the apoptosis of placental trophoblastic cells and its potential mechanism. A pcDNA3.1 expression vector of HBx gene was built and transfected into JEG‐3 and HTR‐8 human placental trophoblastic cell lines, respectively. After transfection for 48 h, RT‐PCR and immunofluorescence analyses showed that HBx mRNA and protein expression was detected in JEG‐3 and HTR‐8 cells. Flow cytometry revealed that early apoptosis of JEG‐3 and HTR‐8 cells was reduced by pcDNA‐HBx transfection. Immunofluorescence and Western blotting showed that PI3K and p‐Akt were significantly upregulated in HTR‐8 cells. HBx ectopic expression did not change the viability of JEG‐3 and HTR‐8 cells when the PI3K/Akt pathway was blocked by its specific inhibitor LY294002. Moreover, the pcDNA‐PI3K expression vector and pcDNA‐HBx were transfected individually or co‐transfected into the cells. The results showed that pcDNA‐PI3K/pcDNA‐HBx co‐transfection promoted the expression of PI3K protein compared with the pcDNA‐PI3K transfection group but did not increase the expression of HBx protein compared with pcDNA‐HBx transfection group. In conclusion, HBx gene can be transferred into JEG‐3 and HTR‐8 human placental trophoblastic cell lines and cause inhibition of cell apoptosis. Its effect of apoptosis inhibition is related to the activation of the PI3K/Akt signaling pathway.