Breast cancer is the most frequent type of cancer in women in Germany. Why cancer cells are so viable is a central research question. Dr. Cristina Cadenas, a researcher at the Leibniz Research Centre for Working Environment and Human Factors (IfADo), and her team have discovered a mechanism by which breast cancer cells use fat to improve their survival. The stronger this survival mechanism, the higher the risk of a negative patient outcome.
Every cell requires nutrients such as carbo- hydrates, proteins and fats to function properly and to divide. The same is true for cancer cells, which are capable of producing fatty acids on their own to enable cell division and tumor growth. Cancer cells are much less adept at doing this under stressful conditions and consequently must ensure their supply of fat in another way, as now determined by Dr. Cristina Cadenas and her team of researchers at the Leibniz Research Centre for Working Environment and Human Factors (IfADo).
Under oxidative stress some breast cancer cells make use of the enzyme endothelial lipase G (LIPG) to supply themselves with fat. These cancer cells produce LIPG and send it to the outer cell membrane where it binds and metabolizes complex fats from the blood stream. Thus, LIPG feeds breast cancer cells with “bite-sized” fatty acids.
Fat protects cells against free radicals
Simultaneously, LIPG helps protect the breast cancer cells against damage by oxidative stress. Oxidative stress develops after accumulation of oxygen radicals that result from metabolic processes or by external factors when environmental toxins enter the body. This can damage cells or even kill them. Cadenas and her team have been able to account for this protective mechanism against cell death by deactivating the LIPG gene so that the breast cancer cells were no longer able to produce LIPG. Without LIPG many of the cells died in response to oxidative stress.
The more LIPG, the higher the risk for further metastases
The researchers were also able to show a significant association between a very high level of LIPG in the tumor and the metastasis-free period of time for the patients. The more fat-splitting enzyme that is produced, the higher the risk of additional metastases, explained IfADo molecular biologist Cristina Cadenas. She proposes that this could be because LIPG protects breast cancer cells from oxidative stress thus aiding cell survival. This connection was observed in patient data in which the primary tumor was surgically removed and there were no metastases present in the lymph nodes. The scientists state that more research is still needed to find out if LIPG deactivation or blocking the fat supply can be used to treat breast cancer.
Dr. Cristina Cadenas Garcia
Leiterin der Nachwuchsgruppe Interorgan-Toxikologie
Phone: + 49 231 1084-392