Interleukin-9 Promotes Pancreatic Cancer Cells Proliferation and Migration via the miR-200aBeta-Catenin Axis

Abstract EN

Background.

Both IL-9 and miR-200a are involved in the pathogenesis of cancers; however, the role of IL-9 in pancreatic cancer and the possible underlying mechanisms remain unknown.

The aim of this study was to investigate the effect of IL-9 on pancreatic cancer cells and its interaction with miR-200a.

Methods.

Pancreatic cancer cells (PANC-1 and AsPC-1) were treated with IL-9 and the expression of miR-200a and β-catenin in pancreatic cancer cells was measured.

β-Catenin was examined as a target gene of miR-200a in pancreatic cancer cells.

The interaction between IL-9 and miR-200a in pancreatic cancer cells was determined by infecting miR-200a mimics prior to IL-9 treatment and then measuring miR-200a and β-catenin expression.

Results.

IL-9 significantly promoted the proliferation, invasion, and migration of pancreatic cancer cells; however, the effect on pancreatic cancer cell apoptosis was insignificant.

β-Catenin was verified as a target gene of miR-200a in pancreatic cancer cells.

Overexpression of miR-200a in pancreatic cancer cells significantly attenuated proliferation and metastasis and reduced β-catenin expression.

IL-9 treatment of pancreatic cancer cells decreased miR-200a expression and increased β-catenin expression.

The effect of miR-200a on pancreatic cancer cells decreased following IL-9 treatment.

Conclusions.

IL-9 promotes proliferation and metastasis in pancreatic cancer cells; this effect may partly involve regulation of the miR-200a/β-catenin axis.