Reviewed by Lily Ramsey, LLMNov 2 2023 The mechanism, which involves the shuttling of messenger RNAs from the nucleus to the cytoplasm, ultimately facilitates DNA repair in cancer cells. These cancer cells can thereby thwart treatments aimed at damaging their DNA.
Previous research had demonstrated that treatment-resistant DLBCL cells often express high levels of a protein called XPO1. In 2019, the U.S. Food and Drug Administration approved a new drug, selinexor, that was designed to target XPO1 and inhibit its activity. The drug, which hinders the growth of lymphoma cells expressing high levels of the protein, is used to treat these refractory cases. Selinexor has helped many, but not all patients with treatment-resistant disease.
However, the investigators found that some of these XPO1-exported proteins are also bound to mRNA molecules; thus, these mRNAs are exported out of the cell nucleus into the cytoplasm where they can be translated into proteins. This new mechanism indicates that the quantity and activity of XPO1 in a cell can therefore affect the expression levels of numerous genes.
Related StoriesTaking some treatment resistant DLBCL cells from patients and grafting them into preclinical models, the researchers found that higher levels of XPO1 ultimately increases the expression of genes that protect cells against death from DNA damage. Inhibiting XPO1 in those models with selinexor increased the lymphomas' sensitivity to DNA-damaging chemotherapies and immune-based treatments.
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