General mechanism for cancer development – Still no drug is available at this level

Green shows the localization of CPEB1 in four tumor cells and blue the nuclei (Credit: © Bava, Méndez, IRB Barcelona)

Green shows the localization of CPEB1 in four tumor cells and blue the nuclei (Credit: © Bava, Méndez, IRB Barcelona)

Researchers have found a general mechanism that speeds up the process of tumor development (cancer development).

This research has been published online in the journal Nature.

Tumor refers to any abnormally developed growth in the body. It can be harmful for the body in the form of cancer or it cannot be a serious issue. Cancer refers to the uncontrolled division of the cells and their growth. One of the main hurdles in the development of the treatment of the cancer is it’s not so-clearly defined mechanisms.

Now the researchers have described that a protein, dubbed as CPEB1 protein – an RNA-binding protein that regulates mRNA translation - affects more than 200 genes that are linked to the rapid increase of the cells (i.e. proliferation) and the gradual advancement of tumors.  This protein has been proposed to control the general regulatory system that increases the spread of cancer.

Researchers have found that CPEB1 reduces the particular region of the RNA that carries most of the signals to determine whether an RNA molecule is made into a protein or not. CPEB1 removes the brakes for hundreds of RNAs thereby increasing the production of proteins. These RNAs have the ability to increase cell dedifferentiation and proliferation. Not only this but this protein accompanies RNA to the cytoplasm for rapid production of the proteins.

“CPEB proteins are necessary during development and also during tissue regeneration via stem cells in adults, but if the programme governed by CPEBs is continually switched on, cells divide when they are not supposed to and form a tumor,” Raúl Méndez, ICREA professor at the Institute for Research in Biomedicine (IRB Barcelona), said in a statement.

“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,” Italian researcher Felice Alessio Bava, first author of the paper, and post-doctoral fellow with Méndez’s group, said.

“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,” Méndez said.

Reference:

Felice-Alessio Bava, Carolina Eliscovich, Pedro G. Ferreira, Belen Miñana, Claudia Ben-Dov, Roderic Guigó, Juan Valcárcel, Raúl Méndez, (2013). CPEB1 coordinates alternative 3′-UTR formation with translational regulation. Nature, doi: 10.1038/nature11901

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