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For fast -growing cancer cells, trying to get enough energy is the top priority,Their cell proliferation and various cell functions are inseparable from energy support.In the past studies, many types will highly rely on the oxidative metabolism of mitochondria to maintain aggressive growth and transfer.This is not difficult to understand. After all, mitochondria is a energy factory of cells, and cancer cells should increase the workload of mitochondria.
Take the acute myelogenesis (AML) as an example. This type of cancer is very invasive and the amplification speed is fast, which is enhanced with them.The mitochondrial function cannot be separated.In response to this rapid proliferation, scientists also believe that mitochondria of AML tumors may be a feasible treatment target.
According to a new study recently published in "Cell-metabolism", scientists from the University of Austin University of Texas found that AML cells will accelerate mitochondrial operation by expanding the "fuel" conveying channel.As a result, more support for tumor growth, and researchers can reasonably reduce the level of specific protein, which can reduce the supply of "fuel" of mitochondria for cancer cells and inhibit the growth of tumors.
According to the paper, the demand for rapidly proliferating cells for oxidized tobaccoicin gonadotrarins (NAD +) is very high, andDuring the oxidation metabolism process, mitochondria became the hub of NAD+.Cancer cells often try to increase the synthetic pathway of NAD+to accelerate proliferation. This is no exception for AML tumors. Many studies have found that the higher the level of NAD+, the stronger AMLs resistance to chemotherapy .
▲ Research diagram (picture source: reference information [1])
But in actual treatment, we cannot directly remove the individuals NAD+, because normal cell function also requires NAD+, which requires us to find and control the special NAD+regulatory in cancer cellsWay.Researchers have found that the transfer protein SLC25A51 just assumes the work of adjusting NAD+, and it will selectively transfer NAD+from cytoplasm to the mitochondria to improve the production level of ATP.
Researchers have obtained some tumor samples from some AML patients. At the same time, they have detected the SLC25A51 level of cells. Compared with normal levels, the SLC25A51 of AML tumor cells has obviously.The higher the level of the SLC25A51 level, the worse their treatment effect.
They tried to knock on the SLC25A51 among various types of leukemia tumors. As a result, the NAD+level in the mitochondria in these cells decreased. At the same time, the proliferation of tumor cells was significantly obviously.inhibition.
▲ Destroy SLC25A51 can reduce the tumor burden of mice (Picture source: Reference materials [1])
In addition to feasible in cell experiments, this strategy is also effective for tumor mice.Mice with AML tumor transplantation at the same time, if the expression of SLC25A51 is reduced, the tumor burden can be observed after about 3 weeks. Compared with the control group, the number of metastatic cancer cells in their spleen is lessThe survival time of mice was extended .This change will not affect other processes of glucose.
At the same time, inhibiting SLC25A51 can be combined with conventional chemotherapy methods to further increase the survival rate of mice. Researchers believe that this is because of the reduction of SLC25A51, which will cause cancer cells to treat chemotherapy drugs for chemotherapy drugsMore sensitive.
The author pointed out that in the future, we need to find a molecule that can safely reduce SLC25A51. It needs to reduce the SLC25A51 to the basic level, but it will not affect normal expression.In this way, it can specifically inhibit the cancer cells of SLC25A51, and will not have side effects on healthy cells.
Reference Data:
[1] ScientistS UNCover Technique to Cut off Cancers Fuel SUPPL. s: //MedicalXPress.com/news/2024-02-scientist-UNCover-TECHNIQUE- CANCER-FUEL.html. Ochondric NAD+/NADHRatio to Control ProLiferation of AML Cells, Cell Metabolism (2024). Doi: 10.1016/J.CMET.2024.01.013
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