Nature: Cancer cells evade the immune system by fighting for methionine, Professor Zhai Weiping proposed the strategy of "depriving methionine and starving cancer cells".

The Journal of Nature published a research paper online by Professor Weiping Z, University of Michigan, USA: Cancer SLC43A2 Alters T cell methionine metabolism and histonemethylation.
the study showed that tumor cells used the highly expressive methionine transport protein SLC43A2 to consume methionine, also known as methionine, competitively preventing T cells from obtaining methionine.
inhibition tumor SLC43A2 restores H3K79me2 histoprotein methylation in T cells, thereby enhancing the immunity of natural anti-tumor immunity or immune checkpoint-induced tumors.
The study identified a mechanism link between methionine metabolism, histamine modification, and T-cell immunity in tumor micro-environments, indicating that the consumption of methionine by cancer cells is a new mechanism of immune escape, and that targeted inhibition of methionine signal transduction can be used as a promising immunotherapy method.
if cancer is made up of pieces of puzzles, the new study stitches together parts of these scattered puzzles to give us a picture of cancer.
in this picture, part of it is made up of the immune system, including why certain immune cells do not function properly in cancer, such as T-cell failure.
other part relates to changes in histoprotein surface modification in immune cells, and the last part relates to the metabolism of amino acids in different cells in cancer.
"No one knows if there's a connection between these issues, and what we're doing is trying to stitch together a few of these challenges and see how they work."
, " said Professor Zhai Weiping.
is one of the pioneers in the exploration of tumor immunosuppression mechanisms and immunotherapy.
his team has made an original contribution to exploring a variety of tumor immune escape mechanisms, including the PD-L1 (B7-H1) pathrapies of tumor patients and their role in tumor therapy.
study illustrates the link between these three questions, suggesting that targeting tumor cell methionine transport proteins can promote immune responses in different tumors.
immune system, T-cells are fighters fighting on the front lines of tumor fighting.
, however, cancer cells can cause abnormalities and malgenescation, preventing T-cells from attacking tumors.
the question is: What causes these anomalies? The researchers studied the micro-environment of the tumor and paid special attention to the tumor's metabolism of T-cell amino acids.
they found that an amino acid called methionine had the greatest effect on the vitality and function of T cells.
low levels of methionine make T cells abnormal, which in turn alters the modification pattern of histoproteins and ultimately leads to impaired T-cell function.
we can imagine that in the tumor micro environment, tumor cells and T cells compete for methionine.
, however, in a brutal and protracted struggle, tumor cells triumphed, resulting in insufficient methionine in T cells to function abnormally and die.
previous study of animal models of immunodeficiency suggests that tumor cells may be addicted to methionine and suggests treatments for "starving" tumor cells by depriving methionine.
, however, says the study suggests it could be a double-edged sword.
" tumor cells compete with T cells for methionine.
T cells need methionine more than tumor cells.
is unlikely to starve all tumor cells, and it is likely to damage and starve T cells.
, we want to be able to selectively inhibit the intake and metabolism of methionine in tumor cells rather than T cells.
, " said Professor Gong.
fact, the study found that supplementing tumor patients with methionine restores T-cell function because high enough methionine means that both tumor cells and T-cells can get enough nutrients.
T-cells control the ultimate fate of the tumor.
is that tumor cells have more transport proteins that transport methionine.
researchers have found that destroying the transport proteins of tumor cells promotes the functional recovery of T cells, which at this point have the ability to obtain enough methionine.
, Professor Gong's team hopes to work with drug experts to try to find a molecular inhibitor that targets methionine metabolism in tumor cells.
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