Recently, cancer researchers at Vanderbilt discovered a new protein that, when genetically regulated to prevent it from interacting with the genes responsible for cancer, will effectively melt tumors within a few days. This exciting research result was recently published in eLife magazine.
You have never heard of the protein that can “melt” tumors!
Professor of Cell Developmental Biology and Biochemistry, Mr. William Tensie, has been dedicated to studying how the oncogene MYC works. MYC promotes the cycle of cell replication and division. The faster the cell grows and divides, the mutations continue to accumulate, leading to The constant growth of tumors. The tumor protein transcription factor MYC is the main driver of malignant tumors, and it is a highly effective but challenging anti-cancer treatment target.
MYC has been an elusive drug target for at least 30 years, and because of its lack of a basic structure, it has been considered by scientists as a “non-drugable” target. In order to solve this obstacle, Professor Tansey started with the protein that interacts with the MYC project, looking for a protein structure that is easier to target than MYC, so as to design mutations that disrupt the interaction between the protein and MYC, thereby preventing cancer growth. If contact between MYC and any protein in the body can be verified, then it can be tracked during cancer treatment.
You have never heard of the protein that can “melt” tumors!
After the 15th day of the experiment, the tumor shrank and disappeared. The cancer cells died within four days. Image Credit: William Tensey
Along this line of thinking, Professor Tansey and his collaborators found the protein host cytokine-1 and determined that it is a clear candidate for this treatment. The contact of HCF1 with MYC is very important for stimulating protein synthesis. When cancer cells with MYC are genetically engineered and no longer interact with HCF1, the cancer cells will begin to self-destruct. Developing a therapy that limits this interaction is a very promising cancer treatment. Professor Tansey said that it is interesting that this does not need to eliminate all the functions of .
HCF-1 is the second protein responsive to MYC discovered by Professor Tansey. The protein WDR5, previously discovered in collaboration with Professor Stephen Fesik of the Orrin H. Ingram II Cancer Institute, has also shown very similar behaviors, and these two The proteins are hidden in obvious places.
MYC binds to DNA to activate genes. Protein transcription factors only need two domains: a DNA binding domain and an activation domain that stimulates DNA to produce RNA and protein. Researchers are currently interested in the part in between, that is, rare proteins that no one has ever studied seriously. After four years of rigorous research, Professor Tansey’s laboratory intends to further understand how HCF1 works with MYC and how it affects the functions of other proteins.
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