HuR confers IL-17a-induced migration and invasion of gastric cancer cells via upregulation of Snail translation

Abstract

Human gastric cancer is a leading cause of cancer mortality in the world wide. We found that the expression of IL-17a was significantly increased in gastric cancer cells. Treatment with recombinant IL-17a (rIL-17a) can increase migration, invasion and epithelial to mesenchymal transition (EMT) of gastric cancer cells. Further, Snail, a key factor to regulate EMT, was significantly increased in rIL-17a-treated gastric cancer cells. While knockdown of Snail can abolish IL-17a-induced EMT of gastric cancer cells. Mechanistically, IL-17a can promote the translation efficiency of Snail, while had no effect on its mRNA expression or protein stability. Further, we found that IL-17a can increase the expression of HuR, which markedly promoted translation of Snail mRNA. While knockdown of HuR can reverse rIL-17a-induced expression of Snail and EMT of gastric cancer cells. Collectively, our data suggested that HuR confers IL-17a induced migration and invasion of gastric cancer cells via upregulation of Snail translation.