PMID- 22093240
OWN - NLM
STAT- MEDLINE
DCOM- 20120120
LR  - 20220317
IS  - 1467-789X (Electronic)
IS  - 1467-7881 (Linking)
VI  - 12
IP  - 12
DP  - 2011 Dec
TI  - Multiple signal pathways in obesity-associated cancer.
PG  - 1063-70
LID - 10.1111/j.1467-789X.2011.00917.x [doi]
AB  - Obesity is increasing worldwide and reaches to a large proportion of the 
      population in developed countries. Thus, obesity-associated cancer has become a 
      major health problem. Multiple cancer risk factors in obesity have been 
      identified including insulin/insulin-like growth factor axis, adipokines and 
      cytokines; and multiple intracellular signal pathways have been studied. However, 
      the role of each signal pathway in obesity-associated cancer is controversial. In 
      this review, the recent studies on signal pathways in obesity-associated cancer 
      are summarized and a unified explanation is provided. Multiple risk factors could 
      initially activate phosphoinositide 3-kinase (PI3K/Akt), mitogen-activated 
      protein kinase (MAPK) and signal transducer and activator of transcription 3 
      (STAT3) pathways. With increased severity of obesity, mammalian target of 
      rapamycin (mTOR), which is down-stream of both PI3K/Akt and MAPK, is highly 
      activated. Activated mTOR in turn inhibits the PI3K/Akt pathway and further 
      activates the STAT3 pathway. This may explain the activation of the PI3K/Akt 
      pathway at the early stage of obesity and its inhibition at the later stage. mTOR 
      inhibition may be used for cancer therapy, but it may be necessary to be combined 
      with the PI3K/Akt inhibitor as decreased mTOR activity will release its feedback 
      inhibition on the PI3K/Akt pathway, which is under the influence of multiple 
      cancer risk factors in obesity. Thus, dual inhibitors of PI3K and mTOR may 
      provide a novel approach.
CI  - (c) 2011 The Author. obesity reviews (c) 2011 International Association for the Study 
      of Obesity.
FAU - Chen, J
AU  - Chen J
AD  - Illawarra Health and Medical Research Institute, University of Wollongong, 
      Wollongong, New South Wales, Australia. jiezhong@uow.edu.au
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20110822
PL  - England
TA  - Obes Rev
JT  - Obesity reviews : an official journal of the International Association for the 
      Study of Obesity
JID - 100897395
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Humans
MH  - Insulin-Like Growth Factor I/metabolism
MH  - MAP Kinase Signaling System/drug effects/*physiology
MH  - *Molecular Targeted Therapy
MH  - Neoplasms/*drug therapy/enzymology
MH  - Obesity/*drug therapy
MH  - STAT3 Transcription Factor/metabolism
MH  - Signal Transduction/drug effects/*physiology
MH  - TOR Serine-Threonine Kinases/antagonists & inhibitors/metabolism
EDAT- 2011/11/19 06:00
MHDA- 2012/01/21 06:00
CRDT- 2011/11/19 06:00
PHST- 2011/11/19 06:00 [entrez]
PHST- 2011/11/19 06:00 [pubmed]
PHST- 2012/01/21 06:00 [medline]
AID - 10.1111/j.1467-789X.2011.00917.x [doi]
PST - ppublish
SO  - Obes Rev. 2011 Dec;12(12):1063-70. doi: 10.1111/j.1467-789X.2011.00917.x. Epub 
      2011 Aug 22.