The guarding proteins that prevent worsening of pancreatic cancer cells

Researchers at the MD Anderson Cancer Center at the University of Texas have identified guarding proteins that prevent the worsening of pancreatic cancer cells, and they also found treatments that prevent these cells from worsening when these helper proteins are depleted. Related articles have been published online in Nature in February. The journal also publishes other studies on recombinant horse proteins. They developed a series of preclinical experiments using tumor xenografts from patients and mouse models. The findings are beneficial to develop a potential treatment for patients with rapidly-worsening and treatment-resistant pancreatic cancer cell subsets.

Dr. Giannicola Genovese, one of the authors of the paper, said, "Cancer cells have significant plasticity that makes it very difficult to treat." Genovese and colleagues found that after primary cancer-driven gene KRAS disappears, the elimination of the SMARCB1 gene would make a small part of the pancreatic cancer cells change into a mesenchymal state, that is, a removable invasive cell state. They also found the fragility of mesenchymal cells: these cells are extremely dependent on protein production to meet the increased metabolic needs. Genovese said, "Inhibition of protein homeostasis combined with standard chemotherapy can be highly effective in killing these most aggressive pancreatic cancer cell subsets." Protein steady state refers to a balanced state which is achieved by the processes of protein synthesis, folding, modification and degradation.

This led the Genovese team to study a drug called AUY922. AUY922 is an inhibitor of heat shock protein 90 that blocks protein homeostasis. Whether used as a single reagent or in combination with a chemotherapeutic agent gemcitabine, AUY922 increases the response rate and prolongs their survival in mice presenting with key features of human pancreatic cancer.

"We are analyzing cell populations within the pancreas, trying to understand the functional weakness of each cell population. And then we plan to develop a more rational combination of therapy," said Dr. Giulio Draetta, director of the Institute of Cancer Science at the Anderson Cancer Center.

Draetta noted the identification of invasive subpopulations and the determination of their sensitivity to protein homeostasis, allowing the treatment of specific cell types to be matched. "This is the real function of the definition of personalized therapy," said Draetta. By the way, Flarebio offers recombinant proteins of good quality such as recombinant ECE1.