Diet-Induced Obesity, Inflammation, and Cancer

JUNG HAN YOON PARK¹*, YOUNG-HEE KANG¹, MI-KYUNG SUNG², DAE YOUNG KWON³ AND YOUNG YANG⁴

1. Department of Food Science and Nutrition, Hallym University, 39 Hallymdaehak-gil, Chuncheon, 200-702, Korea
2. Deparment of Food and Nutriton, Sookmyung Women's University, 52 Hyochangwon-gil, Yongsan-gu, Seoul 140-742, Korea
3. Korea Food Research Institute, 516 Baekhyun-dong, Bundang-gu, Songnam 463-746, Korea
4. Department of Biological Science, Sookmyung Women's University, 52 Hyochangwon-gil, Yongsan-gu, Seoul 140-742, Korea

ABSTRACT

Chronic inflammation plays critical roles in tumor initiation and progression. Inflammatory tumor microenvironment populating tumor cells, inflammatory cells, fibroblasts, and adipocytes and a web of signaling molecules are crucial in the promotion and progression of tumors. Numerous studies have identified transcription factors such as nuclear factor-kappa B, hypoxia-inducible factor-1, and signal transducer and activator of transcription 3 as key modulators in driving inflammation to cancers. Inflammatory cells increase the levels of cytokines that activate these transcription factors to stimulate diverse protumorigenic processes. Additionally, these transcription factors induce production of chemokines that attract more inflammatory cells to maintain tumor-related inflammation. Although the mechanisms by which obesity enhances tumor growth and progression are not clearly defined, population-based studies show that obesity is associated with increased cancer risk. Obesity is associated with a state of chronic low-level inflammation due to the increase in adipocyte sizes as well as residentand recruited-macrophage activities, which alter adipokine profiles. These alterations of adipokine profiles are responsible for
paracrine and endocrine crosstalk with a variety of cell types, thus enhancing tumor growth and progression.

Key words: tumor metastasis, cytokines, chemokines, macrophages, angiogenesis