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• W3145587669 abstract "Oridonin, the main active component of Rab- dosia rubescens, has anti-tumor activities in experimental and clinical settings. The aims of this current study were to explore the anti-cancer abilities of oridonin in hepato- blastoma (HB) HuH-6 cells and to investigate the under- lying mechanisms. We found that oridonin inhibited HuH- 6 cell in vitro growth in a dose- and time-dependent manner. Further, oridonin induced HuH-6 cell apoptosis and G2/M cell cycle arrest. For the mechanism study, we found that oridonin treatment caused endoplasmic reticu- lum (ER) stress activation. Meanwhile, ER stress inhibitor salubrinal or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin's anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin's actions on HuH-6 cells. Oridonin also activated apoptosis signal regulating kinase 1 (ASK1)-c- Jun N-terminal kinase 1 (JNK1) signaling in cultured HuH- 6 cells, which was inhibited by IRE-1 silencing. Impor- tantly, the JNK inhibitors suppressed oridonin-induced growth inhibition and apoptosis in HuH-6 cells. In con- clusion, our results suggest that oridonin induces growth inhibition and apoptosis in cultured HuH-6 cells involving ER stress and ASK1/JNK signaling pathways, which advances our understanding on the molecular mechanisms of oridonin in HB management." @default.
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• W3145587669 date "2013-01-01" @default.
• W3145587669 modified "2023-09-26" @default.
• W3145587669 title "ER stress and ASK1-JNK activation contribute to oridonin- induced apoptosis and growth inhibition in cultured human hepatoblastoma HuH-6 cells" @default.
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