AKT 激活蜗牛诱导的上皮-间质转化，伴随鳞状细胞癌细胞的集体迁移。
AKT primes snail-induced EMT concomitantly with the collective migration of squamous cell carcinoma cells.
机构信息
Department of Oral and Maxillofacial Surgery, Applied Life Sciences, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
出版信息
J Cell Biochem. 2013 Sep;114(9):2039-49. doi: 10.1002/jcb.24545.
In this study, we found that wounding of a confluent monolayer of squamous cell carcinoma (SCC) cells induced epithelial-mesenchymal transition (EMT) specifically at the edge of the wound. This process required the combined stimulation of TGFβ, TNFα, and PDGF-D. Such a combined cytokine treatment of confluent monolayers of the cells upregulated the expression levels of Snail and Slug via PI3K. The PI3K downstream effector, AKT, was dispensable for the upregulation of Snail and Slug, but essential for enabling EMT in response to upregulation of Snail and Slug.
在这项研究中，我们发现，当处于融合状态的鳞状细胞癌细胞单层受到创伤时， EMT 仅在创伤边缘发生。这一过程需要 TGFβ、TNFα 和 PDGF-D 的联合刺激。细胞融合单层接受这种细胞因子联合处理后，PI3K 使 Snail 和 Slug 的表达水平上调。PI3K 的下游效应物 AKT 对于 Snail 和 Slug 的上调并不是必需的，但对于 EMT 的发生却是必需的，因为 Snail 和 Slug 的上调能够促进 EMT 的发生。
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