According to a research published recently in Proceedings of the National Academy of Sciences, Scientists at Rice University in collaboration with other investigators have found that existing drug is able to prevent the overproduction of NAF-1, a protein that plays a role in the proliferation of breast cancer cells. This could open the door for new treatments of breast cancer. The research reveals that decreasing the level of NAF-1 and the activity of the iron-sulfur clusters that it transports could be a potential way of stopping cancer growth. In addition, pioglitazone, a therapeutic agent usually used as a treatment for type 2 diabetes, seems to be able to control NAF-1 production. Furthermore, the research shows that one mutation in NAF-1 prevents cancer cells from proliferating. CusAb offers Recombinant AGTR1 and NAF-1 proteins. Since some other cancers, such as cervical, gastric, liver, laryngeal and prostate cancer, can also express excessive NAF-1, the study could have great implications in the intervene of cancer. NAF-1 belongs to the NEET family of proteins, which are responsible for the transport of clusters of iron and sulfur molecules inside cells. The research showed that excessive NAF-1 in breast cancer tumors helped them to overcome oxidative stress, resulting in larger and more invasive tumors. Moreover, NAF-1 with a single-point mutation blocked the proliferation of cancer cells. Therapeutics that only attach to NAF-1 without affecting other proteins could decrease unwanted adverse effects, noted Rice Dr Fang Bai.
