IL-6 stimulates STAT3 and Pim-1 kinase in pancreatic cancer cell lines

Katherine M. Block, Neale T. Hanke, Erin A. Maine, Amanda F. Baker

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

Objectives: We investigated the signaling pathways activated in response to interleukin 6 (IL-6) in pancreatic cell lines, with a focus on signal transducer and activator of transcription 3 (STAT3) and protooncogene serine/threonine-protein (Pim-1) kinase. Methods: Interleukin 6 receptor (IL-6R) expression and IL-6-induced cell signaling was measured by Western blotting in human pancreatic cell lines. Cucurbitacin I was used as a pharmacological tool to investigate the role of STAT3 in Pim-1 activation. Stably overexpressing Pim-1 kinase cell lines were characterized for their response to IL-6 in vitro and for their growth rate as flank tumors in scid mice. Results: Interleukin 6 receptor was expressed across multiple cancer cell lines. In Panc-1 cells, IL-6 treatment increased expression of phosphorylation of signal transducer and activator of transcription 3 and Pim-1 kinase. Cucurbitacin I treatment alone increased pErk1/2 expression in wild-type and Pim-1-overexpressing cell lines and resulted in exaggerated Pim-1 kinase protein levels in control and IL-6-stimulated cells, suggesting that up-regulation of Pim-1 may be partially STAT3 independent. Pim-1 overexpression did not significantly affect growth rate in vitro or in vivo in Panc-1 or MiaPaCa2 cell lines. Conclusions: Interleukin 6 activates STAT3 and stimulates Pim-1 kinase in pancreatic cell line models. The regulation and consequence of Pim-1 expression seems to be highly context dependent.

Original languageEnglish (US)
Pages (from-to)773-781
Number of pages9
JournalPancreas
Volume41
Issue number5
DOIs
StatePublished - Jul 1 2012

Keywords

  • Interleukin 6
  • Pancreatic cancer
  • Pim-1 kinase
  • Signal transducer and activator of transcription 3

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology

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