Metabolism Link with Breast Cancer

There is evidence that shows a positive correlation between sugar and cancer. This could influence diets for cancer patients and may lead to new therapeutic targets for metabolic diseases and cancer. Characteristic metabolic changes enable cells to meet the demands of cell growth and division. The Warburg effect, also called aerobic glycolysis, is when cancer cells convert glucose to lactate instead of undergoing normal mitochondrial metabolism of glucose. However, the precise mechanism is unclear.

In a recent study, cancer cells were shown to consume more glucose than normal cells, stimulating PFKFB4 kinase activity. The metabolic enzyme, PFKFB4, regulates transcriptional reprogramming by activating the oncogene, SRC-3. The data shows that inhibiting either PFKFB4 or SRC-3 in cancer mice led to the reduced tumor growth and prevented tumors from metastasizing to the lungs. Phosphorylated SRC-3 is commonly overexpressed in breast cancer and plays a key role in regulating gene expression. The phosphorylation of SRC-3 at the Ser857 site was identified as being crucial for metastatic progression. Encouragingly, silencing either SRC-3 or PFKFB-4 in the breast cancer mouse model reduced tumor growth and metastases. This study highlights the interaction between the glycolytic pathway and the oncogenic activation of the transcriptional coactivator SRC-3. Targeting the PFKFB4–SRC-3 interaction may be therapeutically valuable for treatment of breast tumors that are notably dependent on glucose metabolism.

For more information: https://www.nature.com/articles/s41586-018-0018-1

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