Obesity-Induced Peritoneal Dissemination of Ovarian Cancer and Dominant Recruitment of Macrophages in Ascites.
Rosa Mistica C IgnacioEun-Sook LeeAndrew J WilsonAlicia Beeghly-FadielMargaret M WhalenDeok-Soo SonPublished in: Immune network (2018)
One-fifth of cancer deaths are associated with obesity. Because the molecular mechanisms by which obesity affects the progression of ovarian cancer (OC) are poorly understood, we investigated if obesity could promote the progression of OC cells using the postmenopausal ob/ob mouse model and peritoneal dissemination of mouse ID8 OC cells. Compared to lean mice, obese mice had earlier OC occurrence, greater metastasis throughout the peritoneal cavity, a trend toward shorter survival, and higher circulating glucose and proinflammatory chemokine CXCL1 levels. Ascites in obese mice had higher levels of macrophages (Mφ) and chemokines including CCL2, CXCL12, CXCL13, G-CSF and M-CSF. Omental tumor tissues in obese mice had more adipocytes than lean mice. Our data suggest that obesity may accelerate the peritoneal dissemination of OC through higher production of pro-inflammatory chemokines and Mφ recruitment.
Keyphrases
- high fat diet induced
- insulin resistance
- metabolic syndrome
- weight loss
- weight gain
- type diabetes
- induced apoptosis
- mouse model
- adipose tissue
- skeletal muscle
- body mass index
- bone mineral density
- diabetic rats
- oxidative stress
- endothelial cells
- high glucose
- mass spectrometry
- cerebrospinal fluid
- artificial intelligence
- drug induced
- high resolution
- childhood cancer
- glycemic control