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Macrophage migration inhibitory factor is required in concanavalin A‐induced autophagic cell death of human hepatoma (151.9)
Author(s) -
Lai YenChung,
Yeh Trai Ming,
Chuang YungChun
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.151.9
Subject(s) - macrophage migration inhibitory factor , autophagy , concanavalin a , programmed cell death , small hairpin rna , cancer research , microbiology and biotechnology , chemistry , gene knockdown , macrophage , cell , cytokine , biology , immunology , apoptosis , biochemistry , in vitro
Concanavalin A (Con A) is a lectin, which can induce autophagic cell death of hepatoma cells and is considered as an anti‐hepatoma agent. Macrophage migration inhibitory factor (MIF) is a pro‐inflammatory cytokine, which can induce autophagy of hepatoma cells. However, it is unclear whether MIF is required in Con A‐induced hepatoma cell death. In this study, we demonstrated that MIF expression and secretion were increased in Con A‐stimulated human hepatoma cell lines, HepG2 and HuH7. In addition, Con A‐induced autophagy of hepatoma cells was blocked in the presence of MIF inhibitor (ISO‐1). Knockdown of endougenous MIF by small hairpin RNA (shRNA) further confirmed MIF is required in Con A‐induced autophagy of hepatoma cells. These results may explain why lack of MIF can protect mice against Con A‐induced liver injury and suggest the combination of Con A with MIF may represent a better therapy approach against hepatic cancer.