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Snail-induced claudin-11 prompts collective migration for tumour progression.

Nature cell biology (2019-01-22)
Ching-Fei Li, Jia-Yang Chen, Yang-Hui Ho, Wen-Hao Hsu, Liang-Chun Wu, Hsin-Yi Lan, Dennis Shin-Shian Hsu, Shyh-Kuan Tai, Ying-Chih Chang, Muh-Hwa Yang
ABSTRACT

Epithelial-mesenchymal transition (EMT) is a pivotal mechanism for cancer dissemination. However, EMT-regulated individual cancer cell invasion is difficult to detect in clinical samples. Emerging evidence implies that EMT is correlated to collective cell migration and invasion with unknown mechanisms. We show that the EMT transcription factor Snail elicits collective migration in squamous cell carcinoma by inducing the expression of a tight junctional protein, claudin-11. Mechanistically, tyrosine-phosphorylated claudin-11 activates Src, which suppresses RhoA activity at intercellular junctions through p190RhoGAP, maintaining stable cell-cell contacts. In head and neck cancer patients, the Snail-claudin-11 axis prompts the formation of circulating tumour cell clusters, which correlate with tumour progression. Overexpression of snail correlates with increased claudin-11, and both are associated with a worse outcome. This finding extends the current understanding of EMT-mediated cellular migration via a non-individual type of movement to prompt cancer progression.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Imatinib mesylate, ≥98% (HPLC)
Sigma-Aldrich
Imatinib
Sigma-Aldrich
C646, ≥98% (HPLC)
Sigma-Aldrich
Src human, ≥80% (SDS-PAGE), recombinant, expressed in baculovirus infected insect cells, buffered aqueous glycerol solution, histidine-tagged