Platycodin D regulates HAX1 to promote TRAIL apoptosis after interventional liver cancer and induces programmed necrosis in cancer cells

Abstract

Platycodin D (PD) is a tumor suppressor in cancers. However, its role in liver cancer, especially after interventional liver cancer, remains unknown. We detected the expression of HAX-1 after interventional liver cancer by IHC and reverse transcription-polymerase chain reaction, RT-PCR (RT-PCR), and assessed cell proliferation by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, Thiazolyl Blue Tetrazolium Bromide (MTT). PD was down-regulated in CD44+CD24−/low HCC cells. In addition, the results showed that PD could induce Tumor necrosis factor-associated apoptosis-inducing ligands (TRAIL) to be sensitive to apoptosis. HCLS1 associated protein X-1 (HAX-1) is directly regulated by PD in liver cancer cells. We demonstrate that PD promotes apoptosis through mitochondrial/ROS pathway. PD increases TNBCSCs sensitivity to apoptosis via targeting HAX-1 and it might be useful in the treatment of HCC after interventional procedures.