ABSTRACT
Epac, an exchange protein directly activated by cAMP, is a newly discovered guanine nucleotide exchange factor. Epac is a key factor involved in a series of cAMP mediated signaling pathways. Fibrosis disease, a common disease in clinic, usually results from excessive deposition of extracellular matrix under the stimulation of normal physiology (such as aging) or different pathogenetic factors. Epac has been reported to play an important role in fibrotic diseases, so this paper reviews this role of Epac in order to promote the research and development of Epac related mechanisms and drugs.
ABSTRACT
Aim To investigate the effect of ginsen-oside metabolite compound K ( CK) on migration and invasion of human hepatocellular carcinoma line HepG2, and the possible signaling pathway underlying these processes .Methods HepG2 cells were exposed to ginsenoside CK (0, 10, 20, 40, 80 μmol· L-1 ) for 24 h.The cell viability was examined by MTT as-say, and the ability of migration and invasion was ob-served with the wound healing and transwell assay .The expression of E-cadherin , N-cadherin and other related signal molecules such as p-ERK, ERK, p-Akt, Akt were detected by Western blot .Results The cell via-bility was significantly reduced by ginsenoside CK (20, 40, 80 μmol· L-1) (P<0.01).The ability of cell migration and invasion was significantly inhibited after exposure to ginsenoside CK .After treatment with ginsenoside CK (20, 40, 80 μmol · L-1 ) in HepG2 cells, the expression of E-cadherin markedly in-creased, while N-cadherin expression significantly de-creased.Meanwhile, the expression of p-ERK and p-Akt decreased after treated with ginsenoside CK .Con-clusion Ginsenoside CK inhibits the migration and invasion of human hepatocellular carcinoma line HepG2, which may be through suppression of ERK and Akt signaling .