P-Akt/miR‑200 signaling regulates epithelial-mesenchymal transition, migration and invasion in circulating gastric tumor cells.

Both circulating tumor cells (CTCs) and epithelial-mesenchymal transition (EMT) play an important role in invasion, migration and chemoresistant in tumor development. This study aimed to detect whether EMT occurred in human gastric CTCs and to explore the mechanism of EMT in human gastric CTCs. We analysed epithelial markers (pan-CK, E-cadherin), mesenchymal markers (N-cadherin, vimentin) EMT related miR‑200s, and Akt in gastric CTCs. The impact of miR‑200s on EMT, migration and invasion in CTCs was tested. We found that epithelial markers pan-CK, E-cadherin were decreased, and mesenchymal markers N-cadherin, vimentin were overexpressed in gastric CTCs. Expression of EMT related transcriptors, snail1, zeb1, twist1, were reversely correlated with miR‑200s, and were positively correlated with phospho-Akt. Upregulated of miR‑200s downregulated twist1 and zeb1 mRNA expression, and resulted in the supression of EMT, and impaired migration and invasion in gastric CTCs. Inhibition of p-Akt led to upregulation of miR‑200s. In conclusion, gastric CTCs exhibited remarkable EMT process, and p-Akt/miR‑200s signaling regulates EMT, migration and invasion in gastric CTCs.