PMID- 25019059
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20140714
LR  - 20211021
IS  - 2234-943X (Print)
IS  - 2234-943X (Electronic)
IS  - 2234-943X (Linking)
VI  - 4
DP  - 2014
TI  - Putative role of adipose tissue in growth and metabolism of colon cancer cells.
PG  - 164
LID - 10.3389/fonc.2014.00164 [doi]
LID - 164
AB  - Newly emerging data highlight obesity as an important risk factor for developing 
      certain types of cancer, including colorectal cancer. Although evidence supports 
      a link between the two, the mechanisms responsible for this relationship have not 
      yet been fully elucidated. Hypertrophied and dysfunctional adipose tissue of the 
      obese state is characterized by low-grade inflammation. Adipokines and cytokines 
      secreted from adipocytes, together with the abundant availability of lipids from 
      adipocytes in the tumor microenvironment, promote adhesion, migration, and 
      invasion of tumor cells and support tumor progression and uncontrolled growth. 
      One of the predisposed targets of the deleterious effects exerted by secretions 
      from adipose tissue in obesity is the activities associated with the cellular 
      mitochondria. Mitochondrial oxidative metabolism plays a key role in meeting 
      cells' energetic demands by oxidative phosphorylation (OxPhos). Here we discuss: 
      (a) the dynamic relationship between glycolysis, the tricarboxylic acid cycle, 
      and OxPhos; (b) the evidence for impaired OxPhos (i.e., mitochondrial 
      dysfunction) in colon cancer; (c) the mechanisms by which mitochondrial 
      dysfunction can predispose to cancer. We propose that impaired OxPhos increases 
      susceptibility to colon cancer since OxPhos is sensitive to a large number of 
      factors that are intrinsic to the host (e.g., inflammation). Given that 
      adipocytes are a major source of adipokines and energy for the cancer cell, 
      understanding the mechanisms of metabolic symbiosis between cancer cells and 
      adipocytes should reveal new therapeutic possibilities.
FAU - Schwartz, Betty
AU  - Schwartz B
AD  - Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith 
      Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem 
      , Rehovot , Israel.
FAU - Yehuda-Shnaidman, Einav
AU  - Yehuda-Shnaidman E
AD  - Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith 
      Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem 
      , Rehovot , Israel.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140626
PL  - Switzerland
TA  - Front Oncol
JT  - Frontiers in oncology
JID - 101568867
PMC - PMC4071563
OTO - NOTNLM
OT  - Warburg effect
OT  - adipocytokine
OT  - colorectal cancer
OT  - leptin
OT  - mitochondrial dysfunction
EDAT- 2014/07/16 06:00
MHDA- 2014/07/16 06:01
PMCR- 2014/01/01
CRDT- 2014/07/15 06:00
PHST- 2014/02/11 00:00 [received]
PHST- 2014/06/09 00:00 [accepted]
PHST- 2014/07/15 06:00 [entrez]
PHST- 2014/07/16 06:00 [pubmed]
PHST- 2014/07/16 06:01 [medline]
PHST- 2014/01/01 00:00 [pmc-release]
AID - 10.3389/fonc.2014.00164 [doi]
PST - epublish
SO  - Front Oncol. 2014 Jun 26;4:164. doi: 10.3389/fonc.2014.00164. eCollection 2014.