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Ming Li,Pengcheng Sun,Kaikai Dong,Ye Xin,Aslee TaiLulu,Qinyu Li,Jing Sun,Min Peng,Ping Shi 대한약학회 2021 Archives of Pharmacal Research Vol.44 No.2
Chemerin exhibits an inhibitory eff ect on hepatocellularcarcinoma; however, the underlying mechanismis unclear. Here, low chemerin expression was confi rmedin samples of liver cancer patients and hepatoma cells. Chemerin altered hepatoma cell morphology but had noeff ect on normal hepatocytes. Chemerin inhibited proliferationof several human hepatoma cell lines. Real-time PCRdetection of hepatocellular carcinoma markers showed thatmRNA levels of albumin and A-type gamma-glutamyltransferase increased whereas those of alpha-fetoprotein,alkaline phosphatase, B-type gamma-glutamyl transferase,insulin-like growth factor II, and human telomerase reversetranscriptase decreased in chemerin-treated SMMC7721cells. Western blotting revealed that chemerin up-regulatedalbumin and vimentin expressions, and downregulated alpha-fetoprotein expression. Phosphorylated STAT3 wassignifi cantly up-regulated, whereas phosphorylated ERKand AKT were signifi cantly downregulated by chemerin. Chemerin decreased phosphorylated ERK and AKT expressionand the cell proliferation induced by PI3K activator 740Y-P but could not signifi cantly alter phosphorylated STAT3expression and the cell growth induced by STAT3 inhibitorNSC74859. In conclusion, chemerin reversed the malignantphenotype and induced SMMC7721 cell diff erentiation byinhibiting MAPK/ERK and PI3K/AKT signaling; growthinhibition by chemerin is not directly related to the JAK/STAT signaling pathway. Our study provides novel evidencethat chemerin could be utilized for liver cancer treatment.