How to make cancer cells eat themselves?
The receptor for epidermal growth factor (EGFR), located on the membrane of cells, especially cancer cells, not only stimulates cell growth, but also provides them with nutrition. This phenomenon is explained by the connection of the receptor with another transmembrane protein responsible for the transport of glucose into the cell, and it can be used to force the cells to digest themselves.
Isaiah Fiedler and his colleagues from the University of Texas tried to understand the contradictory data obtained from experiments: therapy aimed at inhibiting the cascade of reactions triggered by activation of the receptor to the epidermal growth factor did not lead to the desired result. As the scientists found out, this was explained by an independent effect associated with the supply of glucose to the cell due to the operation of the SGLT1 transport channel. EGFR binds to SGLT1 and prevents the destruction of the latter.
Then the scientists blocked the formation of the EGFR protein using RNA interference - unlike previous experiments, when only intracellular reactions triggered by the receptor were inhibited. This led to the death of prostate cancer cells in in vitro culture.
The analysis showed that this was not due to apoptosis – programmed cell death, but by autophagy – self-digestion due to a lack of nutrients. Scientists have also demonstrated that a controlled decrease in the concentration of EGFR receptors entails a decrease in the amount of SGLT1, followed by a decrease in intracellular glucose concentration. More information about the results of the study can be found in the journal Cancer Cell (Zhang Weihua et al., Survival of Cancer Cells Is Maintained by EGFR Independent of Its Kinase Activity).
The work of Texans not only explains the failures of previous treatment options, but also offers a new way of gene therapy. However, scientists believe that, for a number of practical reasons, it is unlikely to be implemented in the near future.
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