Immune Netw.  2018 Dec;18(6):e47. 10.4110/in.2018.18.e47.

Obesity-Induced Peritoneal Dissemination of Ovarian Cancer and Dominant Recruitment of Macrophages in Ascites

• Ignacio RM
• Lee ES
• Wilson AJ
• Beeghly-Fadiel A
• Whalen MM
• Son DS

• KMID: 2429839
• DOI: http://doi.org/10.4110/in.2018.18.e47

Abstract

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.

Keyword

Obesity; Macrophages; Chemokines; Ascites; Ovarian cancer

MeSH Terms

Adipocytes
Animals
Ascites*
Chemokine CXCL1
Chemokines
Glucose
Granulocyte Colony-Stimulating Factor
Macrophage Colony-Stimulating Factor
Macrophages*
Mice
Mice, Obese
Neoplasm Metastasis
Obesity
Ovarian Neoplasms*
Peritoneal Cavity
Chemokine CXCL1
Chemokines
Glucose
Granulocyte Colony-Stimulating Factor
Macrophage Colony-Stimulating Factor