Presentation Title

The Role of Invadosomes in Neural Crest Cell Migration

Start Date

November 2016

End Date

November 2016

Location

HUB 302-74

Type of Presentation

Poster

Abstract

Neural crest cells (NCCs) are migratory stem cells that arise during early embryonic development. NCCs differentiate to tissues such as bone and cartilage of the face, vascular smooth muscles, and neurons of the gut. In addition, NCCs are suspected to form actin-rich structures known as invadosomes, which allow the cells to remodel and invade tissue as they migrate. The migratory behavior of NCCs, along with their ability to form invadosomes, is reminiscent of the mechanisms used by cancer cells during metastasis. Cancer cells metastasize by forming actin-rich structures known as invadopodia, and migrate from a primary tumor site to colonize new tissues. Due to these similarities, we are investigating the actin-rich invadosomes of NCCs isolated from mouse embryos by immunolabeling and inhibiting key invadopodia proteins such as Src, Tks5, and MT1-MMP. By examining how the inhibition of invadopodia proteins affect invadosome formation and function in NCCs cultured on different matrices, we will show that these structures are analogous to cancer cell invadopodia and that they play a significant role in NCC migration during embryonic development.

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Nov 12th, 1:00 PM Nov 12th, 2:00 PM

The Role of Invadosomes in Neural Crest Cell Migration

HUB 302-74

Neural crest cells (NCCs) are migratory stem cells that arise during early embryonic development. NCCs differentiate to tissues such as bone and cartilage of the face, vascular smooth muscles, and neurons of the gut. In addition, NCCs are suspected to form actin-rich structures known as invadosomes, which allow the cells to remodel and invade tissue as they migrate. The migratory behavior of NCCs, along with their ability to form invadosomes, is reminiscent of the mechanisms used by cancer cells during metastasis. Cancer cells metastasize by forming actin-rich structures known as invadopodia, and migrate from a primary tumor site to colonize new tissues. Due to these similarities, we are investigating the actin-rich invadosomes of NCCs isolated from mouse embryos by immunolabeling and inhibiting key invadopodia proteins such as Src, Tks5, and MT1-MMP. By examining how the inhibition of invadopodia proteins affect invadosome formation and function in NCCs cultured on different matrices, we will show that these structures are analogous to cancer cell invadopodia and that they play a significant role in NCC migration during embryonic development.