PMID- 22554995
OWN - NLM
STAT- MEDLINE
DCOM- 20130214
LR  - 20220316
IS  - 1879-1506 (Electronic)
IS  - 0003-9969 (Linking)
VI  - 57
IP  - 8
DP  - 2012 Aug
TI  - Curcumin-induced autophagy contributes to the decreased survival of oral cancer 
      cells.
PG  - 1018-25
LID - 10.1016/j.archoralbio.2012.04.005 [doi]
AB  - Curcumin, a major active component of turmeric Curcuma longa, has been shown to 
      have inhibitory effects on cancers. In vitro studies suggest that curcumin 
      inhibits cancer cell growth by activating apoptosis, but the mechanism underlying 
      the anticancer effects of curcumin is unclear. Recently, it has been suggested 
      that autophagy may play an important role in cancer therapy. However, little data 
      are available regarding the role of autophagy in oral cancers. In this study, we 
      have shown that curcumin has anticancer activity against oral squamous cell 
      carcinoma (OSCC). Induction of autophagy, marked by autophagic vacuoles 
      formation, was detected by acridine orange staining and monodansylcadaverine 
      (MDC) dye after exposure to curcumin. Conversion of LC3-I to LC3-II, a marker of 
      active autophagosome formation, was also detectable by Western blot following 
      curcumin treatment. We have also observed that curcumin induced reactive oxygen 
      species (ROS) production and autophagic vacuoles formation by curcumin was almost 
      completely blocked in the presence of N-acetylcystein (NAC), an antioxidant. 
      Rescue experiments using an autophagy inhibitor suppressed curcumin-induced cell 
      death in OSCC, confirming that autophagy acts as a pro-death signal. Furthermore, 
      curcumin shows anticancer activity against OSCC via both autophagy and apoptosis. 
      These findings suggest that curcumin may potentially contribute to oral cancer 
      treatment and provide useful information for the development of a new therapeutic 
      agent.
CI  - Copyright (c) 2012 Elsevier Ltd. All rights reserved.
FAU - Kim, Ji Young
AU  - Kim JY
AD  - Department of Oral Pathology, School of Dentistry, Pusan National University, 
      South Korea.
FAU - Cho, Tae Jin
AU  - Cho TJ
FAU - Woo, Bok Hee
AU  - Woo BH
FAU - Choi, Kyung Un
AU  - Choi KU
FAU - Lee, Chang Hun
AU  - Lee CH
FAU - Ryu, Mi Heon
AU  - Ryu MH
FAU - Park, Hae Ryoun
AU  - Park HR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120501
PL  - England
TA  - Arch Oral Biol
JT  - Archives of oral biology
JID - 0116711
RN  - 0 (Antineoplastic Agents)
RN  - 0 (MAP1LC3A protein, human)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Reactive Oxygen Species)
RN  - F30N4O6XVV (Acridine Orange)
RN  - I9N81SC5HD (monodansylcadaverine)
RN  - IT942ZTH98 (Curcumin)
RN  - L90BEN6OLL (Cadaverine)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/pharmacology
MH  - Acridine Orange
MH  - Antineoplastic Agents/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Autophagy/*drug effects
MH  - Blotting, Western
MH  - Cadaverine/analogs & derivatives
MH  - Carcinoma, Squamous Cell/*drug therapy/pathology
MH  - Cell Proliferation/drug effects
MH  - Curcumin/*pharmacology
MH  - Flow Cytometry
MH  - Humans
MH  - Microtubule-Associated Proteins/metabolism
MH  - Mouth Neoplasms/*drug therapy/pathology
MH  - Reactive Oxygen Species/metabolism
MH  - Staining and Labeling
MH  - Tumor Cells, Cultured
MH  - Vacuoles/drug effects
EDAT- 2012/05/05 06:00
MHDA- 2013/02/15 06:00
CRDT- 2012/05/05 06:00
PHST- 2011/08/25 00:00 [received]
PHST- 2012/01/30 00:00 [revised]
PHST- 2012/04/03 00:00 [accepted]
PHST- 2012/05/05 06:00 [entrez]
PHST- 2012/05/05 06:00 [pubmed]
PHST- 2013/02/15 06:00 [medline]
AID - S0003-9969(12)00106-9 [pii]
AID - 10.1016/j.archoralbio.2012.04.005 [doi]
PST - ppublish
SO  - Arch Oral Biol. 2012 Aug;57(8):1018-25. doi: 10.1016/j.archoralbio.2012.04.005. 
      Epub 2012 May 1.