Epidemiological studies have shown that serum
triglyceride (TG) levels are linked with risk of development of
cancer, including colorectal and
pancreatic cancers, and their precancerous lesions. Thus, it is assumed that serum TG plays an important role in
carcinogenesis, and the key
enzyme lipoprotein lipase (LPL), which catalyzes the hydrolysis of plasma TG, may therefore be involved. Dysregulation of LPL has been reported to contribute to many human diseases, such as
atherosclerosis, chylomicronaemia,
obesity, and
type 2 diabetes. Recently, it has been reported that LPL gene deficiency, such as due to chromosome 8p22 loss, LPL gene polymorphism, and epigenetic changes in its promoter region gene, increases
cancer risk, especially in the prostate. In animal experiments, high serum TG levels seem to promote sporadic/
carcinogen-induced genesis of colorectal and
pancreatic cancers. Interestingly,
tumor suppressive effects of LPL inducers, such as
PPAR ligands,
NO-1886, and
indomethacin, have been demonstrated in animal models. Moreover, recent evidence that LPL plays important roles in
inflammation and
obesity implies that it is an appropriate general target for chemopreventive and chemotherapeutic agents.