Overexpression of ankyrin1 promotes pancreatic cancer cell growth

Noriyuki Omura, Masamichi Mizuma, Anne MacGregor, Seung Mo Hong, Michael Ayars, Jose Alejandro Almario, Michael Borges, Mitsuro Kanda, Ang Li, Audrey Vincent, Anirban Maitra, Michael Goggins

Research output: Contribution to journalArticlepeer-review

Abstract

The methylation status of a promoter influences gene expression and aberrant methylation during tumor development has important functional consequences for pancreatic and other cancers. Using methylated CpG island amplification and promoter microarrays, we identified ANK1 as hypomethylated in pancreatic cancers. Expression analysis determined ANK1 as commonly overexpressed in pancreatic cancers relative to normal pancreas. ANK1 was co-expressed with miR-486 in pancreatic cancer cells. Stable knockdown of ANK1 in the pancreatic cancer cell line AsPC1 led to changes in cell morphology, and decreases in colony formation. Stable knockdown of ANK1 also marked reduced the growth of tumors in athymic nude mice. Among patients undergoing pancreaticoduodenectomy, those with pancreatic cancers expressing ANK1 had a poorer prognosis than those without ANK1 expression. These findings indicate a role for ANK1 overexpression in mediating pancreatic cancer tumorigenicity.

Original languageEnglish (US)
Pages (from-to)34977-34987
Number of pages11
JournalOncotarget
Volume7
Issue number23
DOIs
StatePublished - Jun 7 2016

Keywords

  • Ank1
  • Ankyrin
  • Hypomethylation
  • Mir-486
  • Pancreatic cancer

ASJC Scopus subject areas

  • Oncology

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