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Researchers are driving tumor cells to suicide
In addition to heart disease, cancer is the most common cause of death. Treating cancer is particularly difficult when metastases form. This could change soon because an American research team reports a major breakthrough in cancer research. The researchers have apparently discovered an Achilles heel in the cancer cells that can be used to drive the cells to commit suicide.
Scientists at the Perelman School of Medicine discovered a way for tumor cells to self-destruct. They found out in a study that cancer cells produce too much protein and eventually die when a certain protein called ATF4 is blocked. These findings could pave the way for a completely new approach to fighting cancer. The research results were recently presented in the journal Nature Cell Biology.
Genetic research shows new path in cancer treatment
The current research work focuses on the MYC gene. It has been known for years that this gene contributes significantly to uncontrolled tumor growth if it mutates. For this reason, MYC has been assigned a key role in cancer control in several studies. Previous studies have attempted to block the signaling pathways of this gene to stop tumor growth. The Pennsylvania team now found an earlier approach that resulted in the cells killing themselves.
Chain reaction fires tumor growth
MYC is a gene that normally controls cell growth. If it mutates in the context of cancer, it triggers a veritable chain reaction, which leads to uncontrolled growth of cancer cells. Since no way has been found to manipulate the gene directly, previous research was limited to interrupting the chain reaction. However, since the gene controls several processes at the same time, this approach proved to be ineffective.
No more escaping
This is where Constantinos Koumenis' team started. They found an earlier point of attack that suppresses all processes at the same time. This was done by blocking a protein called ATF4 that is involved in all processes of the gene. "We learned that we have to start further downstream to block tumor growth so that cancer cells cannot escape the blockage," explains the study leader.
Is the ATF4 protein the cancer cell Achilles heel?
The research team showed that all signaling pathways of the MYC gene converge on the ATF4 protein. The researchers also recognized that ATF4 activates certain genes that tumors need to grow. The protein also controls the production of other proteins (4E-BP) that are vital for cancer cells to survive.
Cancer cells kill themselves
To test the potential for cancer therapy, the team blocked the ATF4 protein in mice with lymphoma and colon cancer. As a result, the tumor cells continued to produce uncontrolled 4E-BP proteins, but were unable to process them further. The overproduction triggered a stress reaction in the cancer cells, which ultimately led to the death of the cell. This stopped the progression of the cancer in the mice.
Does this also work for people?
Initial tests have already confirmed that ATF4 blocking triggers the same reactions in human tumor cells. This is an indication that this approach could actually be used for cancer therapy. However, it is still unclear what side effects the ATF4 blocking triggers in humans. "We are already working on confirming that this approach will not cause serious side effects," emphasizes the lead author of the Feven Tameire study. In further studies, the ATF4 function will now be examined in more detail in order to develop a new treatment for cancer. (vb)
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Author and source information
This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.
Graduate editor (FH) Volker Blasek
- Perelman School of Medicine: Researchers Identify New Way to Make Cancer Self Destruct (accessed: July 18, 2019), pennmedicine.org
- Tameire, Feven / Verginadis, Ioannis I. / Koumenis, Constantinos / u.a .: ATF4 couples MYC-dependent translational activity to bioenergetic demands during tumor progression, Nature Cell Biology, 2019, nature.com