PMID- 26500073
OWN - NLM
STAT- MEDLINE
DCOM- 20160907
LR  - 20151120
IS  - 1791-2423 (Electronic)
IS  - 1019-6439 (Linking)
VI  - 47
IP  - 6
DP  - 2015 Dec
TI  - Sedanolide induces autophagy through the PI3K, p53 and NF-kappaB signaling pathways 
      in human liver cancer cells.
PG  - 2240-6
LID - 10.3892/ijo.2015.3206 [doi]
AB  - Sedanolide (SN), a phthalide-like compound from celery seed oil, possesses 
      antioxidant effects. However, the effect of SN on cell death in human liver 
      cancer cells has yet to be determined. In this study, cell viability 
      determination, monodansylcadaverine (MDC) fluorescent staining and immunoblot 
      analysis were performed to determine autophagy induction and autophagy-induced 
      protein expression changes via molecular examination after human liver cancer 
      (J5) cells were treated with SN. Our studies demonstrate that SN suppressed J5 
      cell viability by inducing autophagy. Phosphoinositide 3-kinase (PI3K)-I, 
      mammalian target of rapamycin (mTOR) and Akt protein levels decreased, whereas 
      PI3K-III, LC3-II and Beclin-1 protein levels increased following SN treatment in 
      J5 cells. In addition, SN treatment upregulated nuclear p53 and damage-regulated 
      autophagy modulator (DRAM) and downregulated cytosolic p53 and Tp53-induced 
      glycolysis and apoptosis regulator (TIGAR) expression in J5 cells. Furthermore, 
      the cytosolic phosphorylation of inhibitor of kappa B (IkappaB) and nuclear p65 and 
      the DNA-binding activity of NF-kappaB increased after SN treatment. These results 
      suggest that SN induces J5 cell autophagy by regulating PI3K, p53 and NF-kappaB 
      autophagy-associated signaling pathways in J5 cells.
FAU - Hsieh, Shu-Ling
AU  - Hsieh SL
AD  - Department of Seafood Sciences, National Kaohsiung Marine University, Kaohsiung 
      81143, Taiwan, R.O.C.
FAU - Chen, Chi-Tsai
AU  - Chen CT
AD  - Department of Restaurant and Hospitality Management, Chung Hwa University of 
      Medical Technology, Tainan 71703, Taiwan, R.O.C.
FAU - Wang, Jyh-Jye
AU  - Wang JJ
AD  - Department of Nutrition and Health Science, Fooyin University, Kaohsiung 83111, 
      Taiwan, R.O.C.
FAU - Kuo, Yu-Hao
AU  - Kuo YH
AD  - Department of Seafood Sciences, National Kaohsiung Marine University, Kaohsiung 
      81143, Taiwan, R.O.C.
FAU - Li, Chien-Chun
AU  - Li CC
AD  - School of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan, 
      R.O.C.
FAU - Hsieh, Lan-Chi
AU  - Hsieh LC
AD  - Department of Dietetics Kaohsiung Municipal United Hospital, Kaohsiung 80457, 
      Taiwan, R.O.C.
FAU - Wu, Chih-Chung
AU  - Wu CC
AD  - Department of Nutrition and Health Sciences, Chang Jung Christian University, 
      Tainan 71101, Taiwan, R.O.C.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151015
PL  - Greece
TA  - Int J Oncol
JT  - International journal of oncology
JID - 9306042
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Benzofurans)
RN  - 0 (NF-kappa B)
RN  - 0 (TP53 protein, human)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 6415-59-4 (neocnidilide)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
SB  - IM
MH  - Antineoplastic Agents/*pharmacology
MH  - Autophagy/*drug effects/physiology
MH  - Benzofurans/*pharmacology
MH  - Carcinoma, Hepatocellular/metabolism/*pathology
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects
MH  - Humans
MH  - Immunoblotting
MH  - Liver Neoplasms/metabolism/*pathology
MH  - NF-kappa B/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Signal Transduction/*drug effects
MH  - Tumor Suppressor Protein p53/metabolism
EDAT- 2015/10/27 06:00
MHDA- 2016/09/08 06:00
CRDT- 2015/10/27 06:00
PHST- 2015/08/09 00:00 [received]
PHST- 2015/09/26 00:00 [accepted]
PHST- 2015/10/27 06:00 [entrez]
PHST- 2015/10/27 06:00 [pubmed]
PHST- 2016/09/08 06:00 [medline]
AID - 10.3892/ijo.2015.3206 [doi]
PST - ppublish
SO  - Int J Oncol. 2015 Dec;47(6):2240-6. doi: 10.3892/ijo.2015.3206. Epub 2015 Oct 15.