Title : The role and mechanism of ASS1 and urea in the regulation of glycolysis and pyrimidine synthesis by UT-B in B16 cells, respectively
Abstract:
Malignant melanoma is the most malignant skin tumor, which is prone to distant transfer. At present, the research methods are limited, and there is an urgent need to find new treatment targets. The results showed that UT-B overexpression in B16 cells would inhibit the cytosocytical process to inhibit cell proliferation. We found that the expression of ASS1 in B16 cells expressing UT-B was reducd, and it is reported that the glycolysis pathway was inhibited by knockout ASS1 in colorectal cancer. UT-B knockout inhibits urea to discharge extracellular, so urea content in UT-B knockout mice increases.UT-B knockout mice construction B16 tumor model showed that UT-B knockout promoted tumor growth. B16 cells were cultured with urea-containing medium, and the results showed that urea promoted cell proliferation. A number of studies have shown that inhibition of urea circulation promotes pyrimidine synthesis and cell proliferation. It is suggested that the promotion of urea to B16 cells may be achieved by promoting pyrimidine synthesis. Based on this, we guess: 1) The inhibitory effect of UT-B on the glycolysis of B16 cells is achieved by ASS1; 2) UT-B may inhibit cell proliferation by inhibiting cytosine synthesis. This study will start from these two perspectives: the role and mechanism of ASS1 and urea in the regulation of glycolysis and pyrimidine synthesis by UT-B in B16 cells, respectively.
Audience Take Away:
- This is the first report to date describing the role of UT-B protein in the skin.
- We have demonstrated the role of UT-B in the development of cutaneous melanoma and how altered UT-B function severely affects long-term skin health.
- These studies can not only help us understand the development of skin lesions, but also improve our understanding of other cancer types.
