Cancer cells require proteins that bind copper ions in order to develop and spread throughout the human body. Recent studies on the interactions between proteins and how they bind to metals in cancer-related proteins have revealed possible new therapeutic targets.
Small amounts of the metal copper are required by human cells to perform essential biological functions. The conclusion drawn from studies demonstrating higher copper levels in tumor cells and blood serum from cancer patients is that cancer cells require more copper than healthy cells. Additionally, more copper-binding proteins are active when copper levels are higher.
Thus, Pernilla Wittung-Stafshede, professor of chemical biology at Chalmers University of Technology in Sweden, says, “These proteins are highly important to study when it comes to understanding the development of cancer, and deeper knowledge about them can lead to new targets for treatment of the disease.”
The majority of cancer-related deaths are brought on by metastases, or secondary tumors, which develop in various locations throughout the body, such as the liver or lungs. The signaling networks that cancer cells employ to multiply and disseminate across the body include a protein known as Memo1. Previous studies have demonstrated that breast cancer cells’ capacity to metastasize is reduced when the Memo1 gene is inactivated.
A Chalmers research team was interested in learning cancer prevention more about the relationship between copper and Memo1. In a recent study, the researchers used a series of test tube experiments to investigate the Memo1 protein’s capacity to bind copper ions. They learned that the protein exclusively binds copper in its reduced state. This is the most prevalent type of copper ion in living cellst the relationship between copper and Memo1. In a recent study, the researchers used a series of test tube experiments to investigate the Memo1 protein’s capacity to bind copper ions. They learned that the protein exclusively binds copper in its reduced state. This is the most prevalent type of copper ion in living cells. It’s a significant discovery since, despite being required by the body, reduced copper also contributes to redox events that harm or even kill cells. The scientists discovered that Memo1 prevented copper’s harmful redox reactions when it interacted with the metal.
This raises the possibility that the tumor will become heavily dependent on copper because copper can produce chemical reactions that are detrimental to cancer cells. “We think that Memo1 shields the cancer cells so they may survive and proliferate by binding copper when it is needed,” says Pernilla Wittung-Stafshede, a lead author on the study.
The researchers also observed that Memo1 can associate with Atox1, another copper-binding protein that is present in human cells. The research team has previously demonstrated that Atox1, with the aid of copper, contributes to the ability of breast cancer cells to travel and produce metastases. Atox1 is a copper transporter inside human cells. Overall, the results of the current study suggest that targets for cancer prevention treatment in the future may include copper and copper-binding proteins.
“In test tubes, we observed how copper ions might move between the proteins Memo1 and Atox1, and when we examined breast cancer cells, we discovered that the two proteins were spatially adjacent to one another. According to Pernilla Wittung-Stafshede, “this leads us to the conclusion that the exchange of copper between these proteins is biologically relevant and can occur in both cancer cells and test tubes.”
The next step for the researchers is to identify the copper ion binding sites in Memo1 and how the presence of copper affects Memo1’s functions in the development of cancer prevention.
According to Pernilla Wittung-Stafshede, as we increase our fundamental understanding of the function of copper-binding proteins in cancer cells, we also pave the way for new treatments.
The University of York, the University of Gothenburg, and Chalmers University of Technology are all places where the researchers are employed.
The Knut and Alice Wallenberg Foundation, the Swedish Research Council, and Cancerfonden all provided funding for the study.
