A double blow to the thrice negative
How to make the cells of thrice negative breast cancer "starve"
A group of Brazilian researchers has developed a strategy that slows down the growth of triple negative breast cancer cells by depriving them of two main food sources: glutamine and fatty acids, according to a press release from MIT News Measuring chromosome imbalance could clarify cancer prognosis.
Triple negative breast cancer, or TNBC, accounts for approximately 15% to 20% of all breast cancer cases. It is considered the most aggressive type of breast cancer. And it is the most difficult to treat: TNBC cells have neither estrogen receptors, nor progesterone receptors, nor even the HER2 protein, which contributes to the epidermal growth factor. Therefore, this type is called thrice negative and therefore it is difficult to find a medicine against it: drugs that could contact one of the receptors or a protein and disarm them simply have no one to attack. New treatments and new targets are needed to combat TNBC.
One of the methods is to starve a cancerous tumor. Earlier, scientists found out that if you block access to sugar or an alternative energy source – glutamine (an amino acid) to sick cells, then you can slow down the division of cancer cells. However, it turned out that TNBC cells are quite "voracious". The team of Sandra Martha Gomes Dias, a cancer researcher at the National Laboratory of Biological Sciences of Brazil, found out that, in addition to glutamine, triple-negative breast cancer also feeds on fatty acids. According to Diaz, if you simultaneously block the metabolism of glutamine and fatty acids, the growth and migration of TNBC cells slows down.
The drug Telaglenastat, also known as CB-839, prevents the processing of glutamine and is currently undergoing clinical trials for the treatment of TNBC and other types of tumors. CB-839 "turns off" the enzyme glutaminase, which prevents the destruction of cancer cells and benefits from glutamine. However, recent studies have shown that some TNBC cells can resist drug treatment.
To see if changes in gene expression could explain how these cells survive, the study authors exposed TNBC cells to CB-839. So they identified the cells resistant to the drug and those that were sensitive to it, and ordered their RNA.
Scientists have revealed that in the cells that the drug could not kill, the molecular pathways associated with lipid processing were greatly altered. In particular, the levels of the enzymes CPT1 and CPT2, which play an important role in the metabolism of fatty acids, were increased.
CPT1 and 2 act as "gates" for the passage of fatty acids into the mitochondria, where they will be used as fuel for energy production. Brazilian scientists have suggested that if you close these gates, "turning off" CPT1 and simultaneously glutaminase, then TNBC cells resistant to the drug CB-839 will stop multiplying. Such a double blow proved to be very effective.
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