In healthy cells, a protein called MYC helps guide the process of transcription, in which genetic information is converted from DNA into RNA. But when cells turn cancerous, they start to produce way too much MYC, fueling the rapid multiplication of cancerous cells. This MYC overload is a factor in up to 75 percent of all human cancer cases, and the protein’s peculiarly chaotic structure has so far stymied medicine’s attempts to control it.
MYC is “basically a glob of randomness,” said UC Riverside associate professor of chemistry Min Xue. “Conventional drug discovery pipelines rely on well-defined structures, and this does not exist for MYC.”
Last year, Xue’s team published an NIH-funded study describing a win in the fight against MYC’s tricky structure. The discovery revolves around peptides, the molecular building blocks of proteins. The team found that altering the rigidity and shape of a certain peptide helps it bind to MYC and prevent it from fueling the growth of cancer cells. Ultimately, they hit on a novel two-peptide combo that was about a hundred times more effective at targeting and interrupting MYC. Now, they’re working to develop chemistry that improves the peptides’ ability to get inside cells, the next step toward developing a drug based on this research.
Protect life-saving research powered by NIH funding
These promising findings are just the latest results of a longstanding partnership between the federal government and UC scientists. Over generations, this partnership has yielded blockbuster advancements toward the first flu vaccine, the discovery of the role of LDL and HDL cholesterol in heart disease, the invention of modern gene editing, and much, much more.
The cuts to NIH funding proposed by the current administration “will threaten American lives, disrupt time-sensitive life-saving research, and cripple our innovative knowledge-based economy,” said Theresa Maldonado, UC vice president for Research and Innovation.
“Cancer is an awful disease, and we need to continue pushing to find preventions and cures for it,” says professor Masri at UC Irvine. “The only way to move that forward is to learn about the disease, to learn about the mechanistic underpinnings, and then to come up with modalities to target it.”
