title: Interleukin-9 Promotes Pancreatic Cancer Cells Proliferation and Migration via the miR-200a/Beta-Catenin Axis.
abstract: 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 andβ-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 andβ-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 reducedβ-catenin expression. IL-9 treatment of pancreatic cancer cells decreased miR-200a expression and increasedβ-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.
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Bangli
authors.initials: B
authors.lastname: Hu
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Huang
authors.initials: H
authors.lastname: Qiu-Lan
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Rong-E
authors.initials: RE
authors.lastname: Lei
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Cheng
authors.initials: C
authors.lastname: Shi
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Hai-Xing
authors.initials: HX
authors.lastname: Jiang
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Shan-Yu
authors.identifier: 0000-0002-3162-3070
authors.initials: SY
authors.lastname: Qin
mesh_terms: D017209:Apoptosis / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D016906:Interleukin-9 / Q000008:administration & dosage / Q000235:genetics* / Q000378:metabolism*; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D010190:Pancreatic Neoplasms / Q000235:genetics* / Q000473:pathology; D015398:Signal Transduction; D051176:beta Catenin / Q000096:biosynthesis* / Q000235:genetics
chemical_list: C508607:IL9 protein, human; D016906:Interleukin-9; C533896:MIRN200 microRNA, human; D035683:MicroRNAs; D051176:beta Catenin