PMID- 29717538
OWN - NLM
STAT- Publisher
LR  - 20240227
IS  - 1522-7278 (Electronic)
IS  - 1520-4081 (Linking)
DP  - 2018 May 2
TI  - Curcuminoids combined with gefitinib mediated apoptosis and autophagy of human 
      oral cancer SAS cells in vitro and reduced tumor of SAS cell xenograft mice in 
      vivo.
LID - 10.1002/tox.22568 [doi]
AB  - Gefitinib has been used for cancer patients and curcumin (CUR), demethoxycurcumin 
      (DMC), or bisdemethoxycurcumin (BDMC) also shown to induce cancer cell apoptosis. 
      However, no report shows the combination of gefitinib with, CUR, DMC, or BDMC 
      induce cell apoptosis and autophagy in human oral cancer cells. In this study, we 
      investigated the effects of gefitinib with or without CUR, DMC, or BDMC 
      co-treatment on the cell viability, apoptotic cell death, autophagy, mitochondria 
      membrane potential (MMP), and caspase-3 activities by flow cytometry assay and 
      autophagy by acridine orange (AO) staining in human oral cancer SAS cells. 
      Results indicated that gefitinib co-treated with CUR, DMC, or BDMC decreased 
      total viable cell number through the induction of cell apoptosis and autophagy 
      and decreased the levels of MMP and increased caspase-3 activities in SAS cells. 
      Western blotting indicated that gefitinib combined with CUR, DMC, or BDMC led to 
      decrease Bcl-2 protein expression which is an antiapoptotic protein and to 
      increase ATG5, Beclin 1, p62/SQSTM1, and LC3 expression that associated with cell 
      autophagy in SAS cells. Gefitinib combined with CUR and DMC led to significantly 
      reduce the tumor weights and volumes in SAS cell xenograft nude mice but did not 
      affect the total body weights. Based on those observations, we suggest that the 
      combination of gefitinib with CUR, DMC, and BDMC can be a potential anticancer 
      agent for human oral cancer in future.
CI  - (c) 2018 Wiley Periodicals, Inc.
FAU - Hsiao, Yung-Ting
AU  - Hsiao YT
AD  - Department of Biological Science and Technology, China Medical University, 
      Taichung, Taiwan.
FAU - Kuo, Chao-Lin
AU  - Kuo CL
AD  - Department of Chinese Medicine Resources, China Medical University, Taichung 404, 
      Taiwan.
FAU - Lin, Jen-Jyh
AU  - Lin JJ
AD  - Division of Cardiology, China Medical University Hospital, Taichung, Taiwan.
AD  - Department of Respiratory Therapy, China Medical University, Taichung, Taiwan.
FAU - Huang, Wen-Wen
AU  - Huang WW
AD  - Department of Biological Science and Technology, China Medical University, 
      Taichung, Taiwan.
FAU - Peng, Shu-Fen
AU  - Peng SF
AD  - Department of Medical Research, China Medical University Hospital, Taichung, 
      Taiwan.
FAU - Chueh, Fu-Shin
AU  - Chueh FS
AD  - Department of Food Nutrition and Health Biotechnology, Asia University, Wufeng, 
      Taichung, Taiwan.
FAU - Bau, Da-Tian
AU  - Bau DT
AD  - Graduate Institute of Biomedical and Sciences, China Medical University, 
      Taichung, Taiwan.
AD  - Terry Fox Cancer Research Laboratory, Translational Medicine Research Center, 
      China Medical University Hospital, Taichung, Taiwan.
FAU - Chung, Jing-Gung
AU  - Chung JG
AUID- ORCID: 0000-0002-7303-2287
AD  - Department of Biological Science and Technology, China Medical University, 
      Taichung, Taiwan.
AD  - Department of Biotechnology, Asia University, Taichung, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20180502
PL  - United States
TA  - Environ Toxicol
JT  - Environmental toxicology
JID - 100885357
OTO - NOTNLM
OT  - SAS cells
OT  - apoptosis
OT  - autophagy
OT  - bisdemethoxycurcumin
OT  - curcumin
OT  - demethoxycurcumin
OT  - gefitinib
EDAT- 2018/05/03 06:00
MHDA- 2018/05/03 06:00
CRDT- 2018/05/03 06:00
PHST- 2018/01/15 00:00 [received]
PHST- 2018/04/03 00:00 [revised]
PHST- 2018/04/10 00:00 [accepted]
PHST- 2018/05/03 06:00 [entrez]
PHST- 2018/05/03 06:00 [pubmed]
PHST- 2018/05/03 06:00 [medline]
AID - 10.1002/tox.22568 [doi]
PST - aheadofprint
SO  - Environ Toxicol. 2018 May 2. doi: 10.1002/tox.22568.