Details

Autor(en) / Beteiligte

• Sun, Yu
• Tang, Shusheng
• Jin, Xi
• Zhang, Chaoming
• Zhao, Wenxia
• Xiao, Xilong

Titel

Opposite effects of JNK and p38 MAPK signaling pathways on furazolidone-stimulated S phase cell cycle arrest of human hepatoblastoma cell line

Ist Teil von

• Mutation research, 2013-07, Vol.755 (1), p.24-29

Ort / Verlag

Netherlands: Elsevier B.V

Erscheinungsjahr

2013

Quelle

MEDLINE

Beschreibungen/Notizen

• •The effects of furazolidone on S phase cell cycle arrest of HepG2 were studied.•Furazolidone can suppress the cell proliferation of HepG2 in vitro.•Activated p-p38 can inhibit p-JNK activity in HepG2 induced by furazolidone.•FZD induces cell cycle arrest via activating p38 MAPK and inhibiting JNK.•P38 and JNK have opposing effects on FZD-induced S phase cell cycle arrest. Furazolidone (FZD), a synthetic nitrofuran with a broad spectrum of antimicrobial actions, is known to induce genotoxicity and potential carcinogenicity in several types of cells, but little is known about its p38 mitogen-activation protein kinase (p38 MAPK) and c-Jun N-terminal protein kinase (JNK) pathways in human hepatoblastoma cell line (HepG2). Given the previously described essential roles of p38 MAPK and JNK pathways in HepG2 cells, we undertook the present study to investigate the roles of p38 MAPK and JNK pathways in cell cycle arrest of HepG2 cells stimulated with FZD. Here we reported that FZD could obviously induce S phase cell cycle arrest, suppress cell growth, increase the activity of phosphorylated p38 (p-p38), and decrease the activity of phosphorylated JNK (p-JNK) in HepG2 cells. Simultaneously, inhibition of p38 MAPK pathway could significantly reduce FZD-stimulated S phase cell cycle arrest, active cell growth, decrease the activity of p-p38, and increase the activity of p-JNK. To the opposite, inhibition of JNK pathway could significantly increase FZD-stimulated S phase cell cycle arrest, suppress cell growth, decrease the activity of p-JNK, and increase the activity of p-p38. These results demonstrate that JNK and p38 MAPK pathways have opposite roles in FZD-stimulated S phase cell cycle arrest of HepG2 cells. FZD induces S phase cell cycle arrest and suppresses cell proliferation of HepG2 cells via activating the pathway from p38 to p-p38 and inhibiting the pathway from JNK to p-JNK.