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-1α, 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 resident- and 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.
Recommended Citation
Park, J.H.Y.; Kang, Y.-H.; Sung, M.-K.; Kwon, D.Y.; and Yang, Y.
(2012)
"Diet-induced obesity, inflammation, and cancer,"
Journal of Food and Drug Analysis: Vol. 20
:
Iss.
1
, Article 25.
Available at: https://doi.org/10.38212/2224-6614.2091
