Neural crest and cancer: Divergent travelers on similar paths

Abstract

Neural crest cells are multipotent progenitors that dynamically interpret diverse microenvironments to migrate significant distances as a loosely associated collective and contribute to many tissues in the developing vertebrate embryo. Uncovering details of neural crest migration has helped to inform a general understanding of collective cell migration, including that which occurs during cancer metastasis. Here, we discuss several commonalities and differences of neural crest and cancer cell migration and behavior. First, we focus on some of the molecular pathways required for the initial specification and potency of neural crest cells and the roles of many of these pathways in cancer progression. We also describe epithelial-to-mesenchymal transition, which plays a critical role in initiating both neural crest migration and cancer metastasis. Finally, we evaluate studies that demonstrate myriad forms of cell-cell and cell-environment communication during neural crest and cancer collective migration to highlight the remarkable similarities in their molecular and cell biological regulation.

Tracking neural crest cell cycle progression in vivo

“…The neural crest is a unique population of highly migratory stem cells that contributes to the development and formation of multiple tissues in vertebrates (Bronner & LeDouarin, ; Gallik et al, ). Migrating neural crest cells (NCCs) progress through the cell cycle with variable timing, rates, and frequency, the details of which are likely critical for the initiation of migration and maintenance of migratory stream dynamics (Burstyn‐Cohen & Kalcheim, ; Ridenour et al, ).…”

Bimodal function of chromatin remodeler Hmga1 in neural crest induction and Wnt-dependent emigration

“…While well-studied in cancer ( Masciullo et al, 2003 ; Sarhadi et al, 2006 ), little was known about its developmental function in neural crest cells. Given the parallels between the mechanisms that regulate delamination, migration, proliferation, and survival of neural crest cells and tumor cells ( Gallik et al, 2017 ), we sought to characterize the expression of Hmga1 during neural crest development.…”

The in vitro effect of VEGF receptor inhibition on primary alveolar osteoblast nodule formation

“…42 Neural-crestderived and cancer cells are reported to have similar molecular and cell biological regulatory systems. 43 This suggests that osteoblasts cultured from bone harvested from the mandible may offer a more suitable cell population for the study of VEGFR inhibitor targets. 44 This research has used primary HAOBs and found that VEGFR1 was the predominant VEGF receptor present during the osteogenic mineralization process in vitro.…”