The Research Of The Protection Mechanism Of FGF-2Against ER Stress-induced Apoptosis

Researchers reported that a cytoprotective signal transduction pathway known as the "unfolded protein response" or UPR,activated by ER stress, contributes to survival or growth of the cancer cells,such as Hepatocellular carcinoma cell. we knew that Basic fibroblast growth factor, FGF-2, a multi-effect grow factor, is associated with poor prognosis of liver cancer, but there was little information on function of FGF-2in ER stress. In this study, we found that FGF-2can weaken Endoplasmic reticulum stress induced apoptosis through UPR. We show that FGF-2protects the Hepatocellular carcinoma cell line, HepG2and breast cancer cell line, MCF-7from the apoptosis induced by Tunicamycin(a specific inhibitor of N-glycosylation in the ER) or Thapsigargin (non-competitive inhibitor of a class of enzymes known by the acronym SERCA, which stands for sarco/endoplasmic reticulum Ca2+ATPase). We explored the expression of serval proteins and ER molecular chaperoneon transcriptional level and translational level in the Hepatocellular carcinoma cell line. Firstly, we found that FGF-2did not effect Endoplasmic Reticulum stress proteins:BiP, CHOP, GADD34, XBP-1at mRNA level. Secendly our results showed that FGF-2can protect the HepG2cells through down-regulated expression of CHOP/GADD153and Nck-1in protein level, meanwhile Our data suggested that FGF-2could regulate downstream protein of ER stress and MEK/ERK signaling pathway, which may be play central role in HepG2cell resistant ER stress-induced apoptosis.