Dysregulation of the human transforming acidic coiled-coil (TACC) proteins is thought to be important in the evolution of breast cancer and multiple myeloma. However, the exact role of these proteins in the oncogenic process is currently unknown. Using the full-length TACC1 protein as bait to screen a human mammary epithelial cDNA library, we have identified two genes that are also amplified and overexpressed in tumours derived from different cellular origins. TACC1 interacts with the C-terminus of both the microtubule-associated colonic and hepatic tumour overexpressed (ch-TOG) protein, and the oncogenic transcription factor glioma amplified sequence 41/NuMA binding protein 1 (GAS41/NuBI1; where NuMA stands for nuclear mitotic apparatus protein 1). This suggests that the TACC proteins can form multiple complexes, dysregulation of which may be an important step during tumorigenesis.
- breast cancer
- transcription factors
Abbreviations used: ARNT, arylhydrocarbon nuclear translocator; AINT, ARNT interacting protein; ch-TOG, colonic and hepatic tumour overexpressed; DAPI, 4,6-diamidino-2-phenylindole; NuMA, nuclear mitotic apparatus protein 1; GAS41/NuBI1, glioma amplified sequence 41/NuMA binding protein 1; GFP, green fluorescent protein; TACC, transforming acidic coiled-coil; D-TACC, Drosophila TACC; TACIP, TACC-interacting protein.
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