| Literature DB >> 23443559 |
Marie-Laure Fogeron1, Hannah Müller, Sophia Schade, Felix Dreher, Verena Lehmann, Anne Kühnel, Anne-Kathrin Scholz, Karl Kashofer, Alexandra Zerck, Beatrix Fauler, Rudi Lurz, Ralf Herwig, Kurt Zatloukal, Hans Lehrach, Johan Gobom, Eckhard Nordhoff, Bodo M H Lange.
Abstract
Centrosome morphology and number are frequently deregulated in cancer cells. Here, to identify factors that are functionally relevant for centrosome abnormalities in cancer cells, we established a protein-interaction network around 23 centrosomal and cell-cycle regulatory proteins, selecting the interacting proteins that are deregulated in cancer for further studies. One of these components, LGALS3BP, is a centriole- and basal body-associated protein with a dual role, triggering centrosome hypertrophy when overexpressed and causing accumulation of centriolar substructures when downregulated. The cancer cell line SK-BR-3 that overexpresses LGALS3BP exhibits hypertrophic centrosomes, whereas in seminoma tissues with low expression of LGALS3BP, supernumerary centriole-like structures are present. Centrosome hypertrophy is reversed by depleting LGALS3BP in cells endogenously overexpressing this protein, supporting a direct role in centrosome aberration. We propose that LGALS3BP suppresses assembly of centriolar substructures, and when depleted, causes accumulation of centriolar complexes comprising CPAP, acetylated tubulin and centrin.Entities:
Mesh:
Substances:
Year: 2013 PMID: 23443559 DOI: 10.1038/ncomms2517
Source DB: PubMed Journal: Nat Commun ISSN: 2041-1723 Impact factor: 14.919