High-fructose corn syrup is a sweetener manufactured from cornmeal that is found in variety of processed foods. Evidence suggests that high-fructose corn syrup can contribute to breast cancer growth and metastasis. Now a new study has reported that it aides tumor growth in mice.
Foods incorporating high-fructose corn syrup include candy bars, packaged pastries, ketchup, ice cream, soda, juice drinks and a variety of other prepackaged foods. Note that post-diagnostic dietary fructose (from fruit and not added as an ingredient) does not appear to be associated with increased breast cancer mortality risk.
Diets elevated in high-fructose corn syrup have been linked to chronic inflammation, a breast cancer risk factor, as well as increased risk of triple negative (ER-/PR-/HER2-) breast cancer. High-fructose corn syrup has also been reported to worsen the cardiotoxicity induced by the combination of anthracycline chemotherapy plus HER2+ blocking agents.
Breast cancer cell metabolism is characterized by enhanced uptake and use of glucose. Fructose normally is barely metabolized in breast cancer cells. However, it has been demonstrated that when glucose is not available (i.e., the cells are in a state of glucose deficiency), fructose can be used instead by breast cancer cells. The present study reports that the liver converts fructose into usable nutrients for cancer cells. These results suggest that a diet abundant in high-fructose corn syrup could promote the progression of breast cancer.
Latest research finds fructose promotes tumor growth
The study referenced above was designed to investigate the impact of supplemental fructose on tumor growth. The authors first demonstrated that breast cancer, melanoma, and cervical cancer cells have limited ability to use fructose as a nutrient. This appears to be because such cells do not express ketohexokinase-C (KHK-C), the main enzyme responsible for fructose metabolism.
However, fructose supplementation was found to enhance tumor growth in animal models of breast cancer, melanoma, and cervical cancer. This was because the animals' liver cells (hepatocytes) did express KHK-C, which resulted in the metabolism of fructose and the excretion of lysophosphatidylcholines (LPCs).
In co-culture experiments, the authors determined that liver-derived LPCs were consumed by cancer cells and used to generate the major phospholipid of cell membranes. Supplementation of the animals with high-fructose corn syrup increased serum levels of several types of LPC by more than seven times. In addition, administration of LPCs to mice caused increased tumor growth.
Pharmacological inhibition of KHK did not affect cancer cells, but it decreased circulating LPC levels in the animals and prevented fructose-mediated tumor growth. The authors conclude that fructose supplementation increases circulating nutrients such as LPCs that can promote tumor growth.