15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) promotes apoptosis of HBx-positive liver cells

• HBx induces PGE2 accumulation and promotes apoptosis inhibition in HL7702 cells.
• 15d-PGJ2 increases apoptosis rate of HL7702-HBx and HL7702 cells.
• HBx expression causes liver cells to be more sensitive to 15d-PGJ2.
• 15d-PGJ2 may be used for preventing inflammatory changes in liver cells caused by HBV.

This study aims to investigate the inflammatory response characteristics of liver cells caused by HBV x protein (HBx) and the unique function of the PGE2 inhibitor on HBx-positive liver cells. Tetrazolium blue colorimetric method, flow cytometry, and Western blot were performed to detect the proliferation, cycle, and apoptosis protein expression of HBx-positive HL7702 liver and control cells. The effect of the PGE2 inhibitor 15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) on the growth of HL7702-HBx was also observed. HBx induces the PGE2 accumulation in HL7702 liver cells and promotes their growth and inhibits their apoptosis. HL7702-HBx and HL7702 cells showed increased apoptosis rate, increased apoptosis-promoting protein expression, and reduced apoptosis-inhibiting protein expression under the effect of 15d-PGJ2, and the changes in HL7702-HBx cells were more significant than in HL7702 cells. HBx expression causes liver cells to be more sensitive to the apoptosis-promoting function of 15d-PGJ2. Therefore, the use of 15d-PGJ2 may be a new method for the prevention or treatment of inflammatory changes to cancer caused by HBV infection in liver cells.