Obesity is well-known as the second factor for
tumorigenesis after smoking and is bound up with the malignant progression of several kinds of
cancers, including
esophageal cancer,
liver cancer,
colorectal cancer,
kidney cancer, and
ovarian cancer. The increased morbidity and mortality of
obesity-related
cancer are mostly attributed to dysfunctional adipose tissue. The possible mechanisms connecting dysfunctional adipose tissue to high
cancer risk mainly focus on chronic
inflammation,
obesity-related microenvironment,
adipokine secretion disorder, and browning of adipose tissue, and so forth. The stromal vascular cells in adipose tissue trigger chronic
inflammation through secreting inflammatory factors and promote
cancer cell proliferation. Hypertrophic adipose tissues lead to metabolic disorders of adipocytes, such as abnormal levels of
adipokines that mediate
cancer progression and
metastasis.
Cancer patients often show adipose tissue browning and cancerous
cachexia in an advanced stage, which lead to unsatisfied
chemotherapy effect and poor prognosis. However, increasing evidence has shown that adipose tissue may display quite opposite effects in
cancer development. Therefore, the interaction between
cancers and adipose tissue exert a vital role in mediates adipose tissue dysfunction and further leads to
cancer progression. In conclusion, targeting the dysfunction of adipose tissue provides a promising strategy for
cancer prevention and
therapy.