Physiology and pathophysiology of proteinase-activated receptors (PARs)

PAR-2-mediated proliferation of colon cancer cell

Masahiro Nishibori, Shuji Mori, Hideo K. Takahashi

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Proteinase-activated receptor-2 (PAR-2) has been demonstrated to be highly expressed in the gastrointestinal tract. In the present minireview, we summarize the effects of PAR-1 and PAR-2 stimulation using their activating peptides and agonist proteinases on the calcium signaling and the cell proliferation in DLD-1 cell, a human colon cancer cell line. PAR-2 but not PAR-1 stimulation induced the enhancement of cell proliferation, whereas both PAR-1 and PAR-2 stimulation induced the transient increase in [Ca2+]1. PAR-2 stimulation induced the phosphorylation of MEK1/2 and ERK1/2, but PAR-1 stimulation did not. The inhibition of MEK1/2 by PD98059 completely abolished the proliferative response to PAR-2 stimulation. Thus, MEK-ERK activation plays major role in the PAR-2-mediated proliferative response. The coupling of PARs to calcium signaling and MEK-ERK activation may be independent, and varied dependent on cell types.

Original languageEnglish
Pages (from-to)25-30
Number of pages6
JournalJournal of Pharmacological Sciences
Volume97
Issue number1
DOIs
Publication statusPublished - Jan 2005

Fingerprint

Proteinase-Activated Receptors
PAR-2 Receptor
Colonic Neoplasms
PAR-1 Receptor
Calcium Signaling
Mitogen-Activated Protein Kinase Kinases
Cell Proliferation
Gastrointestinal Tract
Peptide Hydrolases
Phosphorylation
Cell Line
Peptides

Keywords

  • Colon cancer
  • Mitogen-activated protein kinase
  • Proliferation
  • Proteinase-activated receptor

ASJC Scopus subject areas

  • Pharmacology

Cite this

Physiology and pathophysiology of proteinase-activated receptors (PARs) : PAR-2-mediated proliferation of colon cancer cell. / Nishibori, Masahiro; Mori, Shuji; Takahashi, Hideo K.

In: Journal of Pharmacological Sciences, Vol. 97, No. 1, 01.2005, p. 25-30.

Research output: Contribution to journalArticle

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