最先端研究セミナー

 

 

Abstract:

It is known that neural crest cells rise from neural/non-neural ectoderm border. Although the mechanism is unknown, the reactive oxygen species (ROS) is accumulated around the border prior to neural crest rising, and coincidentally known cancer players (such as c-Myc, Twist, Snail1/2) start to express in future neural crest region. These processes are quite similar to cancer: The cells having some errors should have been removed by the mechanism such as cell competition, however, cancer primordia express c-Myc for survival, Twist for preventing senescence, and Snails for epithelial mesenchymal transition. Thus, it is still just my view that both the stress and the resistance against the stress may be required for neural crest development and cancer initiation. Recently we reported that a novel pro-apoptotic protein, PLEKHN1 mediated Bax-Bak oligomerization upon the cell death¹. We also found that PLEKHN1 was required for neural crest development. As a second part of my talk, we are going to discuss about collective cell migration and the tissue fluidity of frog neural crest cells³. This concept helped to understand the phenotypes of a gene knockdown in lung adenocarcinoma. The collective migration of cancer cells is still controversial. Although the increase of cell-cell adhesion is thought to prevent cancer dissemination, we observed the opposite phenotypes in vivo analysis and cancer patient specimens². Hopefully my talk gives you some idea how we find the common concept from two very different research areas.

 

Reference:

1. Kuriyama et al., 2018 Cell Death Discovery 4 article number 11 online
2. Kuriyama et al., 2016 Oncogene 35(8): 952-64
3. Kuriyama et al., 2014 Journal of Cell Biology 206 (1):113

 

 

 

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