[Feverfew lactone induces autophagic death of hepatocellular carcinoma SMMC 7721 cells].

OBJECTIVE: To explore the effect and mechanism of feverfew lactone on inducing autophagic death of hepatocellular carcinoma. METHODS: The proliferation of hepatocellular carcinoma SMMC 7721 cells treated with feverfew lactone was measured by MTT assay. The autophagy of SMMC 7721 induced with feverfew lactone was assessed by acridine orange staining, autophagic marker LC3 and p62 detecting and autophagic flows analyzing. In addition, a role of ROS in this process was stated by treatment with antioxidant agent N-acetyl-L-cysteine (NAC). RESULTS: The proliferation of SMMC 7721 cells were inhibited by feverfew lactone in a concentration dependence manner. The expression of LC3 and autophagic flows of SMMC 7721 cells were increased by feverfew lactone, while p62 was decreased, which implied that feverfew lactone could induce the autophagy of SMMC 7721 cells. Further more, the autophagy effect induced by feverfew lactone was declined obviously when treated with NAC suggested that ROS played an important role in this effect. CONCLUSION: Feverfew lactone induces autophagic death of SMMC 7721 cells by stimulating cells to produce ROS. The study will be helpful for the treatment of hepatocellular carcinoma and to provide theoretical basis for the clinical application of feverfew lactone.

[Primary study on preparation and efficiency of neotype hepatocellular carcinoma-dendritic cell vaccine with SOCS1 expression inhibited].

OBJECTIVE: To investigate the effect of SOCS1 expression inhibition on hepatocellular carcinoma-dendritic cell vaccine stimulated by LIGHT. METHODS: The dendritic cells (DC) were generated from mouse bone marrow (BMDC) by cultured in medium containing rmGM-CSF and rmIL-4. The vaccine cells were prepared by loaded with hepatocellular carcinoma HepA antigen and further treated with or without LIGHT and SOCS1 antisense oligonucleotide (AS1). For detecting the maturity of the vaccine cells, the expression of the cell's surface molecules CD40 and CD86 were measured by FACS, and IL-12 and IL-1 secretion from the cells were determined by ELISA. And the CTL activity, cellular proliferation, IL-6 and TNF-beta secretion levels of the vaccine-stimulated lymphocytes were also assessed for analyzing the immune response of lymphocyte. RESULTS: CD40 and CD86 expression of the prepared vaccine cells were obviously enhanced by treatment of LIGHT and AS1, and so were IL-12 and IL-1 (P<0.01). It was also observed that CTL activity, cellular proliferation and IL-6 and TNF-beta secreting levels of lymphocytes that were stimulated by the vaccine cells treated with AS1 were notably enhanced. CONCLUSION: Inhibiting SOCS1 can improve the maturation of hepatocellular carcinoma-DC vaccine cell and can increase its inducing ability of anti-cancer immune response.