While absent from normal epithelia, an actin bundling
protein,
fascin, becomes expressed in invasive
carcinoma of different origins. It is highly enriched at the
tumors' invasive front suggesting that it could play a role in
cancer invasion. Multiple studies have shown that
fascin, through its role in formation of cellular protrusions such as filopodia and invadopodia, enhances
cancer cell migration and invasion in vitro. However, the role of
fascin in vivo remains unknown. We have generated a compound transgenic mouse model that allows expression of
fascin in the intestinal epithelium in the Apc-mutated background. Conditional expression of
fascin led to decrease in mice survival and increase in
tumor burden compared to control animals. Induction of
fascin expression in adult
tumor-bearing animals accelerated
tumor progression and led to formation of invasive
adenocarcinoma. Altogether, our study shows that
fascin can promote
tumor progression in vivo, but also unravels an unexpected role of
fascin in
tumor initiation.