Scientists discovered that blocking a protein slowed cancer growth in mice.
According to RCO News Agency, One of the ways scientists are trying to improve cancer treatments is by better equipping the immune system to fight the disease, and a new study has identified a molecular switch that could do just that.
Through an extensive screening process in which genes in cancer cells were “turned off” in the lab to determine their effects, the researchers discovered that the gene that produces the TAK1 protein is critical for cancer cells to evade immune system attack, according to SA.
Further experiments on cancer cells in mice with normal immune systems confirmed the critical importance of TAK1 to cancer. Tumors in mice without this protein grew more slowly and the mice lived longer on average.
The research team from institutions in Australia and Ireland believe their findings could help develop future treatments. Drugs could potentially target TAK1 production directly and alter this molecular switch.
“We know that TAK1 increases the survival of cancer cells and prevents cell death,” says Anne Huber, a cancer cell biologist at the Olivia Newton-John Cancer Research Institute (ONJCRI) in Australia. However, we did not know that cancer cells use this tactic to avoid being killed by the immune system.
Huber and colleagues investigated the mechanisms underlying TAK1’s effect in more detail. Specifically, this protein protects cancer cells from the activity of CD8⁺ T cells, which are immune cells that clean up damaged cells and destroy deadly invaders like cancer cells.
One of the ways these CD8⁺ T cells are effective is by releasing chemical signals called cytokines that can more easily reach their targets in the absence of TAK1.
Knowing the details of how this process works could help scientists harness it for better cancer treatments. When TAK1 is deleted, cancer cells are essentially trying to survive without one of their best defenders.
It should be emphasized that this study included cancer cells developed in the laboratory and tumors in mouse models. There is reason to believe that these results can be generalized to humans, but this work still needs to be done and extended to a wider range of cancers, while this study focused mainly on melanoma.
However, these findings are encouraging. One of the advantages of immunotherapy approaches to fighting tumors is that they rely more on the body’s own defenses than chemotherapy drugs or radiation.
Patient safety is always a major consideration when it comes to cancer treatments. Stopping the production of TAK1 may be possible in the future, but researchers must determine the potential adverse health effects on the rest of the body and weigh them against the benefits.
Blocking TAK1 could make current immunotherapies more effective by removing this protection from tumors, says ONJCRI medical biologist Tirta Djajawi. TAK1 is also like a shock absorber that allows cancer cells to survive the hardest hits of the immune system, and when we remove it, the tumor collapses under the force of the immune attack.
This research has been published in the journal Cell Reports.
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