News from CEXS-UPF
Researchers at UPF have discovered that the RB protein, responsible for stopping cell proliferation and therefore preventing tumor formation, is activated under cellular stress. The work, led by Eulàlia de Nadal and Francesc Posas, leaders of the research group on Cell Signaling of the DCEXS in collaboration with groups of Baldo Oliva (UPF) and Francisco X. Real (UPF/CNIO), appears in the journal Molecular Cell.
RB (Retinoblastoma) is a tumor suppressor protein that is altered in many cancers. One of the main functions of RB is to inhibit cell cycle progression before genome duplication, so that cell division does not enter until the proper conditions are not met. Therefore, RB prevents cell proliferation under physiological conditions. That is why RB's inactivation may involve the development of cancer, since uncontrolled cellular proliferation results in tumor formation.
The work done by scientists at the Cell Signaling research group has found that RB is also important to stop cell progression in response to cellular stress. Under these conditions, the brake is essential for cell survival. A very remarkable fact is that this new mechanism predominates over others that normally regulate the activity of RB. Therefore, the external activation of this mechanism could be used to block cell division. As Francesc Posas, co-leader of the study says, "this discovery may be relevant in cancer biology because RB is a key protein in cell proliferation and many types of tumor coincide on the inactivation of this protein. If we get to reverse this inhibition, we could stop proliferation."
Gubern A, Joaquin M, Marquès M, Maseres P, Garcia-Garcia J, Amat R, González-Nuñez D, Oliva B, Real FX, de Nadal E* and Posas F*. The N-terminal phosphorylation of RB by p38 bypasses its inactivation by CDKs and prevents proliferation in cancer cells. Molecular Cell. (2016).