Open AccessOverexpression of ankyrin1 promotes pancreatic cancer cell growth
Author(s) -
Noriyuki Omura,
Masamichi Mizuma,
Anne M. Macgregor,
SeungMo Hong,
Michael Ayars,
Jose Alejandro Almario,
Michael Borges,
Mitsuro Kanda,
Ang Li,
Audrey Vincent,
Anirban Maitra,
Michael Goggins
Publication year - 2016
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.9009
Subject(s) - pancreatic cancer , cancer research , cancer , gene knockdown , methylation , dna methylation , medicine , pancreatic tumor , oncology , biology , cell culture , gene expression , genetics , gene
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.