UC Berkeley cancer researchers discover promising target molecule

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A UC Berkeley research team has discovered that a specific molecule inside human cells is responsible for regulating the production of potentially harmful proteins, and by circumventing this regulation, the team was able to halve the invasiveness of lung cancer in tested cells.

The molecule — eukaryotic initiation factor 3, or eIF3 — is part of the process whereby genes are translated into proteins inside cells, specifically the stage of that process involving a type of ribonucleic acid called messenger RNA. According to Jamie Cate — a UC Berkeley professor of biochemistry, biophysics and structural biology who headed the study — unusually large quantities of eIF3 have frequently been found in cancerous cells, which may be because eIF3 produces proteins that are linked to cancer.

“The question we’re asking is when and where are these proteins made,” Cate said. “A lot of work has been done to understand how DNA is translated into RNA, but we’re only just starting to learn about how RNA gets translated to make proteins. That’s where this project comes in.”

According to Cate, eIF3 molecules are able to recognize certain types of messenger RNA that have special “tags” on them, which account for just 500 of the more than 10,000 messenger RNA in a cell. These tagged RNA are responsible for the production of important proteins.

“The eIF3 can increase the amount of protein these RNA make, or it can actually shut down their protein production in some cases,” Cate said. “It’s a sort of control point for cell growth that people (haven’t) appreciated before, and it’s a very interesting target.”

Cate’s team worked on the project for more than two years, during which they attempted to isolate eIF3 from other materials in lung cancer cells to see how the molecule affected the production of potentially cancer-causing proteins.

“Our research shows that we can target the interaction between eIF3 and the 500 tagged RNAs and reduce the invasiveness of cancer,” said Amy Lee, a UC Berkeley postdoctoral student who worked on the research with Cate.

By preventing this interaction from happening, the researchers were able to reduce the cancer’s invasiveness by 50 percent. According to Lee, it is the ability of cancer to spread that poses the most serious threat to patients’ health.

While the results were encouraging, Lee said the actual application of this information about eIF3 to cancer treatment is still “a long way off” because controlling the eIF3 in a human would require a drug that does not yet exist.

“We’ve only just scratched the surface of how this eIF3 works,” Cate said. “The best-case scenario, many years down the road, would be developing molecules that could block these harmful reactions or control them in a beneficial way in order to treat cancer.”

Contact Logan Goldberg at [email protected].