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The sweet tooth of melanoma explained
Published on February 14, 2018
When they become cancerous, cells accelerate their metabolism to become real “sugar addicts”. This behavioral change provides them with a lot of energy, enough to accelerate their growth and multiplication.
But how do they manage to change their eating habits? This is what Professor Philippe Roux’s team from IRIC wanted to know.
To find out, the researchers studied the case of melanoma cells, the most aggressive type among all skin cancers.
In half of the cases, melanoma is caused by a mutation of the BRAF gene which indicates to the cell that it must multiply. In the batch of proteins that BRAF stimulates one was already known to be involved in cancer progression: RSK. Could RSK somehow be involved in telling the cell to increase its sugar intake?
The team immediately focused on PFKFB2, a protein that indirectly increases the sugar requirement of the cell by accelerating its conversion into energy. They had guessed right. The researchers not only proved that RSK stimulates PFKFB2, but they also showed that it is possible to slow the growth of cancer cells by preventing the influence of the former on the latter. Moreover, they showed that this was true in both cultured cells and mice inoculated with cancer cells.
This work was recently the subject of an article published in the journal Cancer Research.
By demonstrating the link that binds PFKFB2 to RSK, and BRAF, Philippe Roux’s team discovered in PFKFB2 a new therapeutic target to tackle melanoma. Preventing this protein from functioning normally should slow the metabolism of cancer cells and at the same time slow down the progression of cancers such as melanoma.
By Martin Primeau