The effects of stimulating protease-activated receptor-1 and -2 in A172 human glioblastoma

Okamoto, Takahiro; Nishibori, Masahiro; Sawada, Ken; Ishibashi, Hiromi; Nakaya, Naoki; Jikuhara, Atsushi; Tanaka, Noriaki; Saeki, Kiyomi

doi:10.1007/s007020170083

Cited by 27 publications

(16 citation statements)

References 49 publications

(49 reference statements)

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“…The result of the literature review is summarized in Tables 1, 2, 3, and 4, (Arora et al 2008;Beaulieu and Church 2007;Bromberg et al 2001;Caruso et al 2006;Cooper et al 2003;Elzer et al 2008;Fujimoto et al 2006;Ghio et al 2006;Granovsky-Grisaru et al 2006;Hazarika et al 2004;Hjortoe et al 2004;Ikeda et al 2003Ikeda et al , 2006Jahan et al 2007;Jin et al 2003;Kang et al 2003;Kaufmann et al 1998Kaufmann et al , 1999Kaufmann et al , 2000Kim et al 2002;Massi et al 2005;Matej et al 2007;Miyata et al 2000;Mize et al 2008;Ohta et al 2003;Okamoto et al 2001;Radjabi et al 2008;Rudroff et al 2002;Sánchez-Hernández et al 2008;Seo et al 2007;Shibata et al 2004;Yoshii et al 2005;Zhang et al 2004). …”

Section: Resultsmentioning

confidence: 96%

Expression of proteinase-activated receptor 1-4 (PAR 1-4) in human cancer

Elste

Petersen

2010

J Mol Hist

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Proteinase activated receptors (PAR 1-4) are membrane receptors with a unique way of activation by proteinases like thrombin, trypsin and matrix metalloproteinases which lead to a specific cellular response. To evaluate the significance of expression and co-expression of PAR in cancer we performed a survey on published data. A Pubmed literature search on "PAR, thrombin, cancer" was performed and 46 publications were selected for systematic review based on the availability of information on tumor type, material type, detection method and specification of positive cases. PAR-1 was found in 77.3% of malignant samples (n = 678), PAR-2 in 79.5% (n = 592), PAR-3 in 12.6% (n = 87) and PAR-4 in 54.9% (n = 153). PAR-1 and -2 were present in adenocarcinomas, melanomas, osteosarcomas, glioblastomas, meningiomas, leukaemias and squamous cell carcinomas. Presence of PAR-3 was limited to kidney and liver cancer. The data on PAR-4 expression was inconclusive. Those studies analysing PAR-1 and PAR-2 reported coexpression of the two receptors. PAR-1 and -2 are widely expressed in human tumors suggesting an important role in tumorigenesis and providing potential targets for therapy. PAR-3 and PAR-4 are less frequently detectable, their expression and potential role in tumorigenesis require further investigation.

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Section: Resultsmentioning

confidence: 96%

Expression of proteinase-activated receptor 1-4 (PAR 1-4) in human cancer

Elste

Petersen

2010

J Mol Hist

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“…Thus, as mentioned above, uncoupling of PAR-1 to the MAP kinase cascade in DLD-1 cells may be the main reason for the lack of growth promotion mediated by PAR-1. In the previous study, we found that PAR-2 stimulation inhibited the proliferation of A172, a human glioblastoma cell line (25). Recent studies demonstrated that PAR-2 activating peptide and trypsin induced the proliferation of pancreatic cancer cells through the stimulation of MAP kinase (26,27).…”

Section: Cell Proliferation and Pars In Other Cellsmentioning

confidence: 89%

Physiology and Pathophysiology of Proteinase-Activated Receptors (PARs): PAR-2-Mediated Proliferation of Colon Cancer Cell

2005

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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 [Ca 2+ ] i . 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.

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“…After SDS-PAGE, the proteins were transferred onto the nitrocellulose membranes and were blotted with antibodies against PAR-2 (Santa Cruz Biotechnology), MEK, MAP kinase, and their phosphorylated forms (Cell Signaling Technology, Beverly, MA, USA). The reaction was developed as described previously (9,16).…”

Section: Immunoblottingmentioning

confidence: 99%

Mast Cell Tryptase Stimulates DLD-1 Carcinoma Through Prostaglandin- and MAP Kinase-Dependent Manners

et al. 2005

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Abstract. We found that striptease-positive mast cells were abundant in the invasive front of human colon adenocarcinoma by examining 30 cases. Because tryptase has been suggested to be the agonist proteinase for protease-activated receptor-2 (PAR-2), we investigated the effects of stimulation of PAR-2 by tryptase on the cell signaling and proliferation of DLD-1, a human colon carcinoma cell line. PAR-2 stimulation by tryptase induced the increase in [Ca 2+ ] i , which was desensitized by the prior application of PAR-2 activating peptide (AP). The proliferative responses of DLD-1 to tryptase and PAR-2 AP were associated with the phosphorylation of MEK and MAP kinase. Inhibition of MEK by PD98059 completely inhibited the proliferationenhancing effects of tryptase and PAR-2 AP as well as phosphorylation of MAP kinase. Moreover, tryptase and PAR-2 AP stimulated the production of prostaglandin E 2 and the inhibition of prostaglandin synthesis by indomethacin or NS398 resulted in the complete inhibition of the proliferative responses to tryptase and PAR-2 AP. Furthermore, the tryptase-stimulated proliferation of DLD-1 was concentration-dependently inhibited by nafamostat mesilate, a specific inhibitor of tryptase. These results as a whole indicated that tryptase has proliferative effects on DLD-1 through cyclooxygenase-and MAP kinase-dependent manners acting on PAR-2 by its proteolytic activity.

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The effects of stimulating protease-activated receptor-1 and -2 in A172 human glioblastoma

Cited by 27 publications

References 49 publications

Expression of proteinase-activated receptor 1-4 (PAR 1-4) in human cancer

Expression of proteinase-activated receptor 1-4 (PAR 1-4) in human cancer

Physiology and Pathophysiology of Proteinase-Activated Receptors (PARs): PAR-2-Mediated Proliferation of Colon Cancer Cell

Mast Cell Tryptase Stimulates DLD-1 Carcinoma Through Prostaglandin- and MAP Kinase-Dependent Manners

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