细胞胆固醇,胰腺癌 z-bo 2020-10-30 418

　　In a recent research report published in the International Journal of Experimental Medicine, scientists from the Cold Spring Harbor Institute and other institutions studied mouse and laboratory-grown pancreatic tissue models to show how cells store cholesterol. We have found that it can be blocked by interfering with the growth and progression of pancreatic cancer cells, and related research results may help develop new therapies for pancreatic cancer. Researcher David Tabeson said he wanted to clarify why pancreatic cancer cells, like many cancer cells, produce a lot of cholesterol. Cholesterol is an essential component of cell membranes. However, the researchers unexpectedly discovered that pancreatic cancer cells far exceed the need to support their growth, because the cholesterol pathway is one of the most common regulatory pathways in the body's metabolism. Cholesterol production is unusual.

　　Most cells produce the required amount of cholesterol. When cholesterol is sufficient, cells will quickly shut down the cholesterol synthesis pathway. However, in this article, we found that it can transform most of the cholesterol produced by cancer cells. It is a form that can be stored in cells, so free cholesterol will not accumulate, but the synthetic pathway will continue to produce free cholesterol. The cancer cells of pancreatic cancer seem to continue to develop based on this excessive synthesis of cholesterol. Researchers believe that a type called SOAT1 (sterol O) allows other molecules to be produced in the same way. -Acyltransferase 1, sterol O-acyltransferase 1) Enzymes, cancer cells can maintain their pathways and maintain daily supplies, while SOAT1 can convert free cholesterol into a storable form.

　　Pancreatic cancer cells are rich in this enzyme. When the researchers removed the SOAT1 enzyme through genetic modification, they found that this method can inhibit the transformation of cancer cells, store cholesterol and prevent the growth of cancer cells at the same time. Animal experiments show that SOAT1 has been removed. Enzymes can prevent tumor growth. More importantly, we found that removing SOAT1 only affected cells with two p53 replication mutations. This genetic change can accelerate the progression of cancer, which is very common in patient tumors. Finally, the researcher Demon said that even without this enzyme, normal pancreatic cells can function normally, making SOAT1 a potential therapeutic target. Researchers hope that new drugs will be developed in the future. It can effectively block the function of SOAT1 enzyme, thereby killing cancer cells without affecting the health of normal cells.