Expression of ROCK-1 in human pancreatic cancer: Its down-regulation by morpholino oligo antisense can reduce the migration of pancreatic cancer cells in vitro

Kenzo Kaneko, Kennichi Satoh, Atsushi Masamune, Akihiko Satoh, Tooru Shimosegawa

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Introduction: Invasion and metastasis of cancer cells require cell motility and adhesion. The small GTPase Rho and one of its effector molecules ROCK regulate cytoskeleton and actomyosin contractility, and play a crucial role in cell adhesion and motility. Results of previous studies showed that the elevated activity of ROCK-1, one of the isomers of ROCK kinases, led to an increase in the activity of invasion and metastasis of cancer cell lines. Aim: To investigate the importance of ROCK-1 in cancer invasion and metastasis. Methodology: We investigated the expression of ROCK-1 in two cancer cell lines and 31 human pancreatic tissues (21 pancreatic cancers [PC] and 10 histologically normal tissues) by immunoblotting and immunohistochemistry. We also examined by haptotaxis assay whether the migratory activity of PC cells could be suppressed by treatment with the morpholino antisense oligonucleotide in vitro. Results: The expression of ROCK-1 was found in 18 of 21 PC tissues (85.7%), but not in normal pancreatic tissues by immunoblotting and immunohistochemistry. Antisense oligo against ROCK-1 significantly inhibited the haptotaxis of Panc-1 in a dose-dependent manner, compared with the control oligo. Conclusion: These results suggest that ROCK-1 may contribute to pancreatic cancer cell invasion and/or metastasis by facilitating cancer cell migration.

Original languageEnglish
Pages (from-to)251-257
Number of pages7
JournalPancreas
Volume24
Issue number3
DOIs
Publication statusPublished - 2002

Keywords

  • Antisense oligonucleotide
  • Invasion
  • Metastasis
  • Pancreatic cancer
  • ROCK
  • Rho-associated kinase

ASJC Scopus subject areas

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

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