Scientists from Harvard Medical School have found that some cancers feed on fat rather than sugars, providing targets for therapy.
Highlights
- Scientists from Harvard Medical School identify certain cancers that feed on fat for energy.
- Prostate cancer and acute myeloid leukemia have been found to feed on fats.
- PHD3 protein controls pathway which controls fat burning.
- Increase of PHD3 in tumor cell lines leads to cell death.
Cancer and Sugar
Cancers are found to feed on sugar molecules and utilize the energy to grow. Cancer cells take up glucose 1-12 times more than normal cells, displaying a very high metabolic rate.
The affinity of cancer cells to sugar molecules is utilized in the Positron Emission Tomography (PET) scan which allows advanced imaging of the body and the identification of cancer cells in the body.
PET is conducted by drinking glucose labeled with radioactive material which is carried by the body to all its parts. The glucose is preferentially picked up by the tumor cells which are detected by imaging systems. This helps in identifying the presence of cancer cells in the body.
Cancer cells break down the glucose molecules at a faster rate than normal cells, utilizing the energy as fuel.
Scientists from the Harvard School of Medicine have found that some cancers could be using fat as fuel, changing the perception on cancers. In a normal human, carbohydrates and sugars are first broken down into smaller units and utilized for energy, storing fats for use when sugars are not available. There exist specific signaling pathways that block the utilization of fat for fuel.
The protein prolyl hydroxylase 3 (PHD3) is found to regulate fat burning by blocking pathways that are utilized to break down fats. The scientists found that in cancers like prostate cancer and acute myeloid leukemia, this protein was found to be in low concentration.
Fat burning in normal humans is triggered when there is a low concentration of sugars or when the energy levels are low. This can lead to the activation of a protein called AMP-activated protein kinase (AMPK) that further activates the enzyme acetyl CoA carboxylase (ACC). This leads to the burning of fat. The body holds on to its fat even under considerable stress as it is the storehouse of energy and to help the body tide over possible episodes of lack of nutrition. However, this could be reversed in certain forms of cancer, according to Harvard Medical School Scientists.
Evidence to Support that Certain Cancers Utilized Fats
Experiment to suppress PHD3: The scientists carried out experiments where the protein PHD3 was suppressed, they found that this protein suppressed and modified ACC2, preventing the burning of fat.
Researching previous data: The scientists studied data related to cancers and found that cancers that depended on sugar had high level of PHD3 while cancers that depended on fats had low level of PHD3.
Testing effect of PHD3 on tumor cell Lines: In an effort to understand the importance of PHD3 on tumor cell lines of mice, it was found that
- Cancer cells stopped growing
- Further, the cancer cells died
The study holds promise for therapy that can be aimed at starving certain cancers which will arrest their growth and lead to their termination. However, there are considerable steps to take before this study will be available for human therapy, though the promises they offer are plenty.
Reference:
- 5 Reasons Cancers and Sugars are Best Friends - (http://beatcancer.org/blog-posts/5-reasons-cancer-and-sugar-are-best-friends/)