MicroRNA, hsa-miR-200c, is an independent prognostic factor in pancreatic cancer and its upregulation inhibits pancreatic cancer invasion but increases cell proliferation

Jun Yu, Kenoki Ohuchida, Kazuhiro Mizumoto, Norihiro Sato, Tadashi Kayashima, Hayato Fujita, Kouhei Nakata, Masao Tanaka

Research output: Contribution to journalArticle

Abstract

Background: Recently, the microRNA-200 family was reported to affect cancer biology by regulating epithelial to mesenchymal transition (EMT). Especially, the expression of miR-200c has been shown to be associated with upregulating the expression of E-cadherin, a gene known to be involved in pancreatic cancer behavior. However, the significance of miR-200c in pancreatic cancer is unknown.Methods: In the present study, we investigated the relationship between E-cadherin and miR-200c expression in a panel of 14 pancreatic cancer cell lines and in macro-dissected formalin-fixed paraffin-embedded (FFPE) tissue samples obtained from 99 patients who underwent pancreatectomy for pancreatic cancer. We also investigated the effects of miR-200c on the proliferation and invasion of pancreatic cancer cells.Results: We found that patients with high levels of miR-200c expression had significantly better survival rates than those with low levels of miR-200c expression. We also found a remarkably strong correlation between the levels of miR-200c and E-cadherin expression.Conclusions: These data indicate that miR-200c may play a role in the pancreatic cancer biology and may be a novel marker for the prognosis of pancreatic cancer.

Original languageEnglish (US)
Article number169
JournalMolecular Cancer
Volume9
DOIs
StatePublished - Jun 28 2010

ASJC Scopus subject areas

  • Molecular Medicine
  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'MicroRNA, hsa-miR-200c, is an independent prognostic factor in pancreatic cancer and its upregulation inhibits pancreatic cancer invasion but increases cell proliferation'. Together they form a unique fingerprint.

  • Cite this