Sabio lab

at the CNIC

Tag: cancer (page 1 of 5)

¿De qué mueren los extremeños?

«Aunque la supervivencia del cáncer ha aumentado hasta superar el 50% de forma global, la incidencia y la mortalidad siguen al alza por el envejecimiento de la población», explica Guadalupe Sabio, científica del Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), que incide también en que «los tratamientos de las afecciones circulatorias cada vez son mejores y se está consiguiendo aumentar la supervivencia de los pacientes tras, por ejemplo, un ataque de miocardio».

[Read more in El Periódico Extremadura]

Nuclear Receptors and Cancer (3-4 December 2019)

Guadalupe Sabio is giving a talk at the seminar on Nuclear Receptors and Cancer that will be held at the Instituto de Investigaciones Biomédicas Alberto Sols (Madrid, Spain).

There is no registration fee, but the attendance is limited to 75 participants.

Nuclear Receptors and Cancer 2019

p38γ is essential for cell cycle progression and liver tumorigenesis

Antonia Tomás-Loba, Elisa Manieri, Bárbara González-Terán, Alfonso Mora, Luis Leiva-Vega, Ayelén M. Santamans, Rafael Romero-Becerra, Elena Rodríguez, Aránzazu Pintor-Chocano, Ferran Feixas, Juan Antonio López, Beatriz Caballero, Marianna Trakala, Óscar Blanco, Jorge L. Torres, Lourdes Hernández-Cosido, Valle Montalvo-Romeral, Nuria Matesanz, Marta Roche-Molina, Juan Antonio Bernal, Hannah Mischo, Marta León, Ainoa Caballero, Diego Miranda-Saavedra, Jesús Ruiz-Cabello, Yulia A. Nevzorova, Francisco Javier Cubero, Jerónimo Bravo, Jesús Vázquez, Marcos Malumbres, Miguel Marcos, Sílvia Osuna & Guadalupe Sabio.

The cell cycle is a tightly regulated process that is controlled by the conserved cyclin-dependent kinase (CDK)–cyclin protein complex. However, control of the G0-to-G1 transition is not completely understood.

Mitosis in liver
Mitosis in hepatocytes (Photo: Alfonso Mora/CNIC).

Here we demonstrate that p38 MAPK gamma (p38γ) acts as a CDK-like kinase and thus cooperates with CDKs, regulating entry into the cell cycle. p38γ shares high sequence homology, inhibition sensitivity and substrate specificity with CDK family members. In mouse hepatocytes, p38γ induces proliferation after partial hepatectomy by promoting the phosphorylation of retinoblastoma tumour suppressor protein at known CDK target residues.

Lack of p38γ or treatment with the p38γ inhibitor pirfenidone protects against the chemically induced formation of liver tumours. Furthermore, biopsies of human hepatocellular carcinoma show high expression of p38γ, suggesting that p38γ could be a therapeutic target in the treatment of this disease.

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