PMID- 25026276
OWN - NLM
STAT- MEDLINE
DCOM- 20151120
LR  - 20211021
IS  - 1949-2553 (Electronic)
IS  - 1949-2553 (Linking)
VI  - 5
IP  - 15
DP  - 2014 Aug 15
TI  - Dietary energy balance modulates ovarian cancer progression and metastasis.
PG  - 6063-75
AB  - A high energy balance, or caloric excess, accounts as a tumor promoting factor, 
      while a negative energy balance via caloric restriction, has been shown to delay 
      cancer progression. The effect of energy balance on ovarian cancer progression 
      was investigated in an isogeneic immunocompetent mouse model of epithelial 
      ovarian cancer kept on a regimen of regular diet, high energy diet (HED) and 
      calorie restricted diet (CRD), prior to inoculating the animals intraperitoneally 
      with the mouse ovarian surface epithelial ID8 cancer cells. Tumor evaluation 
      revealed that mice group on HED displayed the most extensive tumor formation with 
      the highest tumor score at all organ sites (diaphragm, peritoneum, bowel, liver, 
      kidney, spleen), accompanied with increased levels of insulin, leptin, insulin 
      growth factor-1 (IGF-1), monocyte chemoattractant protein-1 (MCP-1), VEGF and 
      interleukin 6 (IL-6). On the other hand, the mice group on CRD exhibited the 
      least tumor burden associated with a significant reduction in levels of insulin, 
      IGF-1, leptin, MCP-1, VEGF and IL-6. Immunohistochemistry analysis of tumors from 
      HED mice showed higher activation of Akt and mTOR with decreased adenosine 
      monophosphate activated kinase (AMPK) and SIRT1 activation, while tumors from the 
      CRD group exhibited the reverse profile. In conclusion, ovarian cancer growth and 
      metastasis occurred more aggressively under HED conditions and was significantly 
      curtailed under CRD. The suggested mechanism involves modulated secretion of 
      growth factors, cytokines and altered regulation of AMPK and SIRT1 that converges 
      on mTOR inhibition. While the role of a high energy state in ovarian cancer has 
      not been confirnmed in the literature, the current findings support investigating 
      the potential impact of diet modulation as adjunct to other anticancer therapies 
      and as possible individualized treatment strategy of epithelial ovarian cancer.
FAU - Al-Wahab, Zaid
AU  - Al-Wahab Z
AD  - Division of Gynecology Oncology, Wayne State University, Detroit, MI.
FAU - Tebbe, Calvin
AU  - Tebbe C
AD  - Department of Women's Health, Obstetrics and Gynecology, Wayne State University, 
      Detroit, MI.
FAU - Chhina, Jasdeep
AU  - Chhina J
AD  - Department of Women's Health, Obstetrics and Gynecology, Wayne State University, 
      Detroit, MI.
FAU - Dar, Sajad A
AU  - Dar SA
AD  - Department of Women's Health, Obstetrics and Gynecology, Wayne State University, 
      Detroit, MI.
FAU - Morris, Robert T
AU  - Morris RT
AD  - Division of Gynecology Oncology, Wayne State University, Detroit, MI.
FAU - Ali-Fehmi, Rouba
AU  - Ali-Fehmi R
AD  - Department of Pathology, Karmanos Cancer Institute, Wayne State Univeristy, 
      Detroit, MI.
FAU - Giri, Shailendra
AU  - Giri S
AD  - Department of Neurology, Henry Ford Hospital, Detroit, MI.
FAU - Munkarah, Adnan R
AU  - Munkarah AR
AD  - Department of Women's Health, Obstetrics and Gynecology, Wayne State University, 
      Detroit, MI.
FAU - Rattan, Ramandeep
AU  - Rattan R
AD  - Department of Women's Health, Obstetrics and Gynecology, Wayne State University, 
      Detroit, MI.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Oncotarget
JT  - Oncotarget
JID - 101532965
SB  - IM
MH  - Animals
MH  - Carcinoma, Ovarian Epithelial
MH  - Disease Progression
MH  - Female
MH  - Humans
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neoplasm Metastasis
MH  - Neoplasms, Glandular and Epithelial/diet therapy/*metabolism/*pathology
MH  - Ovarian Neoplasms/diet therapy/*metabolism/*pathology
MH  - Phosphorylation
MH  - Signal Transduction
PMC - PMC4171613
COIS- Authors have no conflicts of interest to report.
EDAT- 2014/07/16 06:00
MHDA- 2015/12/15 06:00
PMCR- 2014/08/01
CRDT- 2014/07/16 06:00
PHST- 2014/07/16 06:00 [entrez]
PHST- 2014/07/16 06:00 [pubmed]
PHST- 2015/12/15 06:00 [medline]
PHST- 2014/08/01 00:00 [pmc-release]
AID - 2168 [pii]
AID - 10.18632/oncotarget.2168 [doi]
PST - ppublish
SO  - Oncotarget. 2014 Aug 15;5(15):6063-75. doi: 10.18632/oncotarget.2168.