Nature: Metabolism and Tumors - Diabetes Therapy Can Also Treat Tumors

Recently, the international top journal nature published the latest research findings from the Elsa R. Flores research team of the Anderson Cancer Research Center in the United States on the tumor growth of IAPP-driven metabolic reprogramming to inhibit p53 deletion.

The researchers point out that changes in TP53 usually occur in human tumors, and previous studies have shown that reactivation of TP53 in mice can inhibit tumor growth. But it turns out that the strategy of re-activating TP53 is very difficult to implement, so the researchers tried to find another strategy to inhibit tumor growth by regulating TP53 with the family proteins TP63 and TP73. The TA subtypes of p63 and p73 are structurally and functionally similar to p53, but the ΔN subtype of p63 and p73 (deletion of the acid transactivation domain) is usually overexpressed in cancer, mainly in p53, TA63 and TA73. Loss of function inhibits their anti-tumor function. The p53 family of proteins can influence a variety of processes in the cell to inhibit tumor function, such as apoptosis and autophagy, so understanding the interaction between p53 family proteins and various cellular processes is important for treating tumors by changing p53 signaling pathway. .

Researchers such as Avinashnarayan Venkatanarayan found that this leads to intracellular metabolic reprogramming by p63 or p73 ΔN subtype deletion and inhibits p53-deficient tumor growth by up-regulating IAPP. IAPP encodes amylin and inhibits cell glycolysis and induces ROS production and apoptosis via calcitonin receptor (CalcR) and receptor activity modifying protein 3 (RAMP3). At the same time, the researchers also found that pramlintide (currently used to treat type I and type II diabetes) can cause rapid inhibition of p53-deficient thymic lymphoma.

Taken together, this paper found that deletion of the ΔN subtype of p53 homologous proteins p63 and p73 up-regulates IAPP expression, drives metabolic reprogramming in tumor cells, and inhibits p53-deficient tumor growth by inducing ROS production and apoptosis. The new role of pramlintide in the inhibition of thymic lymphoma has also been found to be of great importance in the development of new drugs for the treatment of tumors.

Original link: http://news.bioon.com/article/6665411.html