Abstract
Endothelin (ET) is a vasoconstrictor peptide originally isolated from vascular endothelial cells. Recent studies have revealed that ET has many biological functions including growth factor-like activity. The present study aims to clarify whether ET-1 possesses the ability to stimulate anchorage-independent cellular growth, an indicator of factors with transforming activity. We found that NRK 49F cells possess a large number of high-affinity ET-1 receptors; labeled 125I-ET-1 binding was displaced by unlabeled ET-2 in a similar dose response, but in the case of ET-3, 100-fold more was required. Specific 125I-ET-3 binding was undetectable in NRK 49F cells, indicating that ET receptors in NRK 49F cells are ET-1/ET-2 selective. NRK 49F is a cell line which is most commonly used to assay for anchorage-independent cellular growth. Therefore, we explored whether ETs promote anchorage-independent cellular growth in this cell line. ET-1 and ET-2 stimulated NRK colony formation dose dependently in the presence of 1 nM epidermal growth factor (EGF). In contrast, ET-3 did not have colony-stimulating ability. In the presence of EGF, the maximal effect of ET-1 was approximately 90% of that of transforming growth factor-β. Moreover, in the presence of maximal stimulating concentrations of EGF and transforming growth factor-β, ET-1 additionally induced colony formation. These results indicate that ET-1 and -2 possess transforming growth factor-like activity for NRK 49F cells. Since ET-1 and -2 increased intracellular calcium levels, this ion may participate in signal transduction pathways by which ET-1 and -2 promote colony formation.
| Original language | English |
|---|---|
| Pages (from-to) | 3011-3014 |
| Number of pages | 4 |
| Journal | Cancer Research |
| Volume | 52 |
| Issue number | 11 |
| Publication status | Published - 1992 Jun 1 |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Stimulation of anchorage-independent cell growth by endothelin in NRK 49F cells. / Kusuhara, Masatoshi; Yamaguchi, Ken; Kuranami, Masaru; Suzaki, Ai; Ishikawa, Shiro; Moon, Hanlim; Adachi, Isamu; Hori, Shingo; Handa, Shunnosuke.
In: Cancer Research, Vol. 52, No. 11, 01.06.1992, p. 3011-3014.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Stimulation of anchorage-independent cell growth by endothelin in NRK 49F cells
AU - Kusuhara, Masatoshi
AU - Yamaguchi, Ken
AU - Kuranami, Masaru
AU - Suzaki, Ai
AU - Ishikawa, Shiro
AU - Moon, Hanlim
AU - Adachi, Isamu
AU - Hori, Shingo
AU - Handa, Shunnosuke
PY - 1992/6/1
Y1 - 1992/6/1
N2 - Endothelin (ET) is a vasoconstrictor peptide originally isolated from vascular endothelial cells. Recent studies have revealed that ET has many biological functions including growth factor-like activity. The present study aims to clarify whether ET-1 possesses the ability to stimulate anchorage-independent cellular growth, an indicator of factors with transforming activity. We found that NRK 49F cells possess a large number of high-affinity ET-1 receptors; labeled 125I-ET-1 binding was displaced by unlabeled ET-2 in a similar dose response, but in the case of ET-3, 100-fold more was required. Specific 125I-ET-3 binding was undetectable in NRK 49F cells, indicating that ET receptors in NRK 49F cells are ET-1/ET-2 selective. NRK 49F is a cell line which is most commonly used to assay for anchorage-independent cellular growth. Therefore, we explored whether ETs promote anchorage-independent cellular growth in this cell line. ET-1 and ET-2 stimulated NRK colony formation dose dependently in the presence of 1 nM epidermal growth factor (EGF). In contrast, ET-3 did not have colony-stimulating ability. In the presence of EGF, the maximal effect of ET-1 was approximately 90% of that of transforming growth factor-β. Moreover, in the presence of maximal stimulating concentrations of EGF and transforming growth factor-β, ET-1 additionally induced colony formation. These results indicate that ET-1 and -2 possess transforming growth factor-like activity for NRK 49F cells. Since ET-1 and -2 increased intracellular calcium levels, this ion may participate in signal transduction pathways by which ET-1 and -2 promote colony formation.
AB - Endothelin (ET) is a vasoconstrictor peptide originally isolated from vascular endothelial cells. Recent studies have revealed that ET has many biological functions including growth factor-like activity. The present study aims to clarify whether ET-1 possesses the ability to stimulate anchorage-independent cellular growth, an indicator of factors with transforming activity. We found that NRK 49F cells possess a large number of high-affinity ET-1 receptors; labeled 125I-ET-1 binding was displaced by unlabeled ET-2 in a similar dose response, but in the case of ET-3, 100-fold more was required. Specific 125I-ET-3 binding was undetectable in NRK 49F cells, indicating that ET receptors in NRK 49F cells are ET-1/ET-2 selective. NRK 49F is a cell line which is most commonly used to assay for anchorage-independent cellular growth. Therefore, we explored whether ETs promote anchorage-independent cellular growth in this cell line. ET-1 and ET-2 stimulated NRK colony formation dose dependently in the presence of 1 nM epidermal growth factor (EGF). In contrast, ET-3 did not have colony-stimulating ability. In the presence of EGF, the maximal effect of ET-1 was approximately 90% of that of transforming growth factor-β. Moreover, in the presence of maximal stimulating concentrations of EGF and transforming growth factor-β, ET-1 additionally induced colony formation. These results indicate that ET-1 and -2 possess transforming growth factor-like activity for NRK 49F cells. Since ET-1 and -2 increased intracellular calcium levels, this ion may participate in signal transduction pathways by which ET-1 and -2 promote colony formation.
UR - http://www.scopus.com/inward/record.url?scp=0026734649&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026734649&partnerID=8YFLogxK
M3 - Article
C2 - 1317255
AN - SCOPUS:0026734649
VL - 52
SP - 3011
EP - 3014
JO - Cancer Research
JF - Cancer Research
SN - 0008-5472
IS - 11
ER -