t which have specific activities in diseased states. "This finding is positive from a therapeutic viewpoint because it means that if you remove CPEB1 from healthy cells, its function can be taken over by any other CPEB protein. In contrast, in tumors only CPEB1 has the capacity to shorten these regions, thus affecting only tumor cells", states Italian researcher Felice Alessio Bava, first author of the paper, and post-doctoral fellow with Mndez's group who, this year, has obtained his doctorate degree through the "la Caixa" International Fellowship Programme. This study provides further evidence of the potential of CPEB proteins as therapeutic targets. In 2011, in a study published in
Nature Medicine, Mndez identified that CPEB4 "switches on" hundreds of genes linked to tumor growth. This new study explains that the overexpression of CPEB4 in tumors is because CPEB1 has also "released the brakes that keep CPEB4 at low levels in a healthy tissue". "The fact that these proteins control each other is also advantageous from a therapeutic point of view", asserts Mndez, "because partial inhibition, by a drug, would be amplified, thus allowing tumor cell reprogramming. The amplification should make it easier to find a viable compound".
The lab has developed a system to screen therapeutic molecules for a drug that can inhibit the action of CPEB in tumors while having few secondary effects on healthy cells. "There is no drug currently available that influences the regulation of gene expression at this level. Our findings open up a pioneering therapeutic window. We are optimistic about the potential of CPEB proteins as targets", says Mndez.
The action of CPEB proteins should be considered in the design of other therapeutic strategies
The study published in Nature includes a meticulous genomic analysis of RNA molecules that are processed in different ways depending on whether CPBE1 is present. The study provides a list of between 200 a
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