Researchers at the University of California, San Francisco (UCSF) have uncovered the mechanism by which zotatifin, a drug currently under clinical investigation, inhibits cancer cell proliferation. Their study reveals that zotatifin targets the eukaryotic initiation factor 4A (eIF4A), an enzyme responsible for unwinding messenger RNA (mRNA) molecules, a critical step in protein synthesis. In cancer cells, eIF4A is often overactive, leading to the excessive production of proteins that drive tumor growth. Zotatifin binds to eIF4A, effectively converting it into a molecular brake that prevents the translation of oncogenic mRNAs into proteins. This action disrupts the uncontrolled protein production characteristic of cancer cells, thereby inhibiting their growth.
In preclinical models, zotatifin demonstrated significant efficacy against prostate cancer. Mice treated with the drug exhibited not only halted tumor progression but also tumor regression. The inhibition of eIF4A by zotatifin led to a marked decrease in the synthesis of proteins essential for cancer cell survival and proliferation. These promising results suggest that zotatifin could be a valuable therapeutic agent for various cancers characterized by dysregulated protein synthesis. Further clinical trials are underway to evaluate its safet Click for More Details
