LGALS3BP regulates centriole biogenesis and centrosome hypertrophy in cancer cells.

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.
Mesh Terms:
Animals, Antigens, Neoplasm, Carrier Proteins, Cell Line, Tumor, Centrioles, Chromatography, Affinity, Extracellular Matrix Proteins, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Glycoproteins, HEK293 Cells, Humans, Hypertrophy, Male, Microtubules, Neoplasms, Protein Interaction Maps, Protein Transport, Protein-Serine-Threonine Kinases, RNA, Small Interfering, Rats, Rats, Sprague-Dawley, Seminoma, Spindle Apparatus, Tumor Markers, Biological
Nat Commun
Date: Feb. 28, 2013
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