Solve the 100-year-old problem of cancer cell "energy plants"

2021 is the centennial of a fundamental discovery that is taught in every biochemistry textbook. In 1921, German doctor Otto Wahlberg observed that cancer cells get energy from glucose in a strangely inefficient way: cancer cells "burn" glucose without oxygen, but ferment it like yeast. This oxygen-free process occurs quickly, but most of the energy in glucose is not used.
years, various hypothotics have been put forward to explain the Vass effect, including that cancer cells have mitochondrial defects and therefore cannot control the burning of glucose, but these explanations cannot stand the test of time.
Now, based on a large number of genetic and biochemical experiments, a team of immunologists led by Ming Li of the Sloan-Kettering Institute has come up with an answer that boils down to the link between watts' metabolism and the activity of powerful enzymes (PI3 kinases) in cells. The results were published recently in Science.
"PI3 kinase is a key signaling molecule that functions almost like the commander-in-chief of cell metabolism. Li said, "Most energy-consuming cell events, including cell division, occur only when pi3 kinase signals. "
as cells metabolize, the activity of PI3 kinase increases, which in turn enhances the "determination" of cell division. This is similar to the commander-in-chief's megaphone.
this finding corrects the widely held view among biochemists that metabolism is a secondary part of cell signaling. They also believe that targeted metabolism may be an effective way to stop cancer from growing.
team studied the watts of immune cells, which also rely on this seemingly inefficient form of metabolism. When immune cells are warned of an infection, a specific cell called T cells changes from a typical form of aerobic metabolism to Ava's metabolism because their numbers are increasing and the mechanisms to fight infection are enhanced.
key "switch" to control this transition is an enzyme called lactic acid dehydrogenase A (LDHA), which is conducted in response to PI3 kinase signals. As a result of this conversion, glucose only partially decomposes, and cellular sol rapidly produces cellular energy called ATP. Instead, when cells use oxygen to burn glucose, partially decomposed molecules reach the mitochondrials and break down further there, delaying the production of ATP.
team found that in mice, T cells lacking LDHA were not able to maintain pi3 kinase activity and therefore were not effective against infection. This means that this metabolic enzyme controls the signal activity of the cells.
like other kinases, PI3 kinases rely on ATP to function. Since ATP is a net product of Watts metabolism, a positive feedback loop is established between Watts metabolism and PI3 kinase activity to ensure the continued activity of PI3 kinase, thus ensuring cell division.
as to why activated immune cells prioritize this metabolism, Li suspects this is related to the mechanism by which cells need to produce ATP quickly to speed up cell division and fight infection. The positive feedback loop ensures that once the program starts, it continues until the infection is eradicated.
, PI3 kinase is one of the most active signaling pathways in cancer. Like immune cells, cancer cells may use Watts metabolism to maintain the activity of this signaling path, ensuring its continued growth and division. The findings raise the interesting possibility of inhibiting the growth of cancer cells by blocking the activity of LDHA. (Source: Wang Fang, China Science Journal)
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