Protein may help control cancer cells

The protein eIF4A3 may hold the key for future cancer treatments, Karolinska researchers find.


Scientists at the Swedish Karolinska Institutet have investigated the role of the protein eIF4A3 in the growth of cancer cells. Their study in the journal Science Advances shows that by blocking or reducing the production of this protein, other processes arise that cause the growth and cell division of cancer cells to cease and eventually die.

The researchers at the Department of Medical Biochemistry and Biophysics reduced the production of eIF4A3 in cultured cancer cells. The inhibition of the protein altered the manufacturing process of proteins by disrupting ribosome biogenesis, and thereby inhibited the growth of cancer cells.
There were two distinct changes in the cancer cells. “Firstly, we saw that the blocking of eIF4A3 activated the protein p53, a protein that has an important role to play in fighting cancer cells,” explained Dimitris Kanellis, first author of the study. “Interestingly, we noted that the blocking eIF4A3 also meant that the MDM2 protein changed. This change helps to maintain and strengthen p53 and can be beneficial when we want to inhibit the growth of cancer cells.”

The researchers now hope that their findings will open up new opportunities for better and more effective treatment of cancer patients. “The discovery is very relevant as this type of targeted treatment may represent a new possible approach in chemotherapy, for example in colon cancer where cancer cells often have a high level of ribosomes and rapid growth. Another example is a sarcoma, cancer of the body’s support tissues, where we know that sometimes there is an overproduction of MDM2. This increases the chances of more effective treatment,” commented Mikael Lindström and professor Jiri Bartek, corresponding authors in the study.

“There may also be synergies between the chemical compounds that block eIF4A3 and drugs that are already used to treat cancer that we will now research further,” concluded Lindström.


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