C. elegans as a model to study cancer, in Genetics and Nature Medicine journals

The nematode Caernorhabditis elegans is used in Dr. Julián Cerón’s laboratory as a model for several diseases. The group has recently published two articles, in Genetics and in Nature medicine.

The article in Genetics is the result of the thesis by the Austrian student Iris Ertl, directed by Dr. Cerón. Iris and collaborators have studied, by means of genetic, transcriptomic and proteomic techniques, two mutually exclusive proteins of the SWI/SNF complex that are highly conserved from yeast to human. The human homologues of such proteins (SMARCD1, SMARCD2 and SMARCD3) have been described as deregulated in different types of tumour, and this work in C. elegans helps to unravel the specificities of the pathologies related to these proteins, suggesting the study of synthetic lethal interactions as therapeutic approach. The physical and functional interaction between components of the SWI/SNF components and proteins from the nuclear envelope are among the most interesting findings.

On the other hand, in a work leaded by Dr. López Otín from Universidad de Oviedo and published in Nature Medicine, the alteration of AIRAPL has been described to cause proliferative neoplasm through a mechanism depending on the insulin pathway. Dra. Montserrat Porta, from the C. elegans core facility, performed longevity and RNAi assays to show that the functional interplay between AIRAPL and the insulin pathway takes place already in worms. With these data, C. elegans turns into a preclinical model to study such functional relationship.

References to articles:

Functional Interplay of Two Paralogs Encoding SWI/SNF Chromatin-Remodeling Accessory Subunits During Caenorhabditis elegans Development. Ertl I, Porta-de-la-Riva M, Gómez-Orte E, Rubio K, Aristizábal-Corrales D, Cornes E, Fontrodona L, Osteikoetxea X, Ayuso C, Askjaer P, Cabello J, Cerón J*. Genetics. 2016 Jan 6. pii: genetics.115.183533.

Loss of the proteostasis factor AIRAPL causes myeloid transformation by deregulating IGF-1 signaling. Osorio FG, Soria-Valles C, Santiago-Fernández O, Bernal T,2, Mittelbrunn M, Colado E, Rodríguez F, Bonzon-Kulichenko E, Vázquez J, Porta-de-la-Riva M, Cerón J, Fueyo A Li J, Green AR1, Freije JM, López-Otín C. Nature Medicine. 2016 Jan;22(1):91-6.

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