PMID- 16630125
OWN - NLM
STAT- MEDLINE
DCOM- 20060619
LR  - 20220310
IS  - 1347-9032 (Print)
IS  - 1347-9032 (Linking)
VI  - 97
IP  - 4
DP  - 2006 Apr
TI  - Curcumin targets Akt cell survival signaling pathway in HTLV-I-infected T-cell 
      lines.
PG  - 322-7
AB  - The Akt signaling pathway is important for survival and growth of cancer cells. 
      In the present paper we show that the Akt signaling pathway is constitutively 
      activated in human T-cell leukemia virus type I (HTLV-I)-infected T-cell lines 
      and in primary adult T-cell leukemia (ATL) cells. Curcumin, a natural compound 
      present in turmeric, has been studied vigorously as a potent chemopreventive 
      agent for cancer therapy because of its inhibitory effect on proliferation and 
      induction of apoptosis in several tumor cell lines. We investigated the effect of 
      curcumin on Akt activity in HTLV-I-infected T-cell lines and primary ATL cells. 
      Phosphorylated PDK1 is an activator of Akt by phosphorylating Akt. Curcumin 
      reduced phosphorylation of PDK1 and inhibited constitutive activation of Akt. 
      Curcumin activated glycogen synthase kinase (GSK)-3beta, a downstream target of 
      Akt kinase, by inhibiting phosphorylation of this protein. Curcumin reduced the 
      expression of cell cycle regulators, cyclin D1 and c-Myc proteins, which are both 
      degraded by activated GSK-3beta. Our results suggest that activation of the Akt 
      signaling pathway plays an important role in ATL cell survival, and that curcumin 
      may have anti-ATL properties mediated, at least in part, by inhibiting Akt 
      activity. We propose that Akt-targeting agents could be useful for the treatment 
      of ATL. In this regard, curcumin is a potentially promising compound for the 
      treatment of ATL.
CI  - (Cancer Sci 2006; 97: 322 - 327).
FAU - Tomita, Mariko
AU  - Tomita M
AD  - Division of Molecular Virology and Oncology, Graduate School of Medicine, 
      University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan.
FAU - Matsuda, Takehiro
AU  - Matsuda T
FAU - Kawakami, Hirochika
AU  - Kawakami H
FAU - Uchihara, Jun-Nosuke
AU  - Uchihara JN
FAU - Okudaira, Taeko
AU  - Okudaira T
FAU - Masuda, Masato
AU  - Masuda M
FAU - Ohshiro, Kazuiku
AU  - Ohshiro K
FAU - Mori, Naoki
AU  - Mori N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Retracted Publication
PL  - England
TA  - Cancer Sci
JT  - Cancer science
JID - 101168776
RN  - 0 (Antineoplastic Agents)
RN  - EC 2.7.11.1 (GSK3B protein, human)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
RN  - IT942ZTH98 (Curcumin)
SB  - IM
RIN - Nakamura Y. Cancer Sci. 2011 Feb;102(2):498. PMID: 21265953
MH  - Antineoplastic Agents/*pharmacology
MH  - Cell Survival/*drug effects
MH  - Curcumin/*pharmacology
MH  - Glycogen Synthase Kinase 3/metabolism
MH  - Glycogen Synthase Kinase 3 beta
MH  - Human T-lymphotropic virus 1/*drug effects
MH  - Humans
MH  - Phosphorylation/drug effects
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - *Signal Transduction
MH  - T-Lymphocytes/drug effects/*virology
MH  - Tumor Cells, Cultured/virology
EDAT- 2006/04/25 09:00
MHDA- 2006/06/20 09:00
CRDT- 2006/04/25 09:00
PHST- 2006/04/25 09:00 [pubmed]
PHST- 2006/06/20 09:00 [medline]
PHST- 2006/04/25 09:00 [entrez]
AID - CAS [pii]
AID - 10.1111/j.1349-7006.2006.00175.x [doi]
PST - ppublish
SO  - Cancer Sci. 2006 Apr;97(4):322-7. doi: 10.1111/j.1349-7006.2006.00175.x.