Concurrent overexpression of Ets-1 and c-Met correlates with a phenotype of high cellular motility in human esophageal cancer

Hiroshi Saeki, Shinya Oda, Hidetoshi Kawaguchi, Shinji Ohno, Hiroyuki Kuwano, Yoshihiko Maehara, Keizo Sugimachi

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Hepatocyte growth factor (HGF) stimulates cell motility as well as mitotic activity of cells. High concentrations of HGF or overexpression of its cellular receptor c-Met in cancer have been reported. We analyzed the expression status of c-Met immunohistochemically in 76 cases of human esophageal cancer. Overexpression of c-Met was noted at a considerably high frequency. Intriguingly, c-Met overexpression was frequent in a specific type of cell nest formation in tumors, i.e., the small nest type, in which tumors form small, dispersed cell nests. Further immunohistochemical analyses using serial sections revealed a striking coincidence between overexpression of c-Met and its transcriptional factor, Ets-1. Overexpression of c-Met and Ets-1 was statistically more frequent in small nest type tumors. The close correlation in expression status between Ets-1 and c-Met was also confirmed using 6 established human esophageal cancer cell lines. In addition, cells that expressed high levels of Ets-1 and c-Met exhibited an extremely motile phenotype by HGF stimulation in vitro. The presence of HGF in tissue sections was confirmed using similar immunohistochemical approaches. These observations suggest that in human esophageal cancer cells the transcriptional factor Ets-1 upregulates the expression of c-Met and, consequently, confers on cells a highly motile phenotype leading to a specific form of tumor development.

Original languageEnglish
Pages (from-to)8-13
Number of pages6
JournalInternational Journal of Cancer
Volume98
Issue number1
DOIs
Publication statusPublished - Mar 1 2002

Fingerprint

Esophageal Neoplasms
Hepatocyte Growth Factor
Phenotype
Neoplasms
Cell Movement
Up-Regulation
Cell Line

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Concurrent overexpression of Ets-1 and c-Met correlates with a phenotype of high cellular motility in human esophageal cancer. / Saeki, Hiroshi; Oda, Shinya; Kawaguchi, Hidetoshi; Ohno, Shinji; Kuwano, Hiroyuki; Maehara, Yoshihiko; Sugimachi, Keizo.

In: International Journal of Cancer, Vol. 98, No. 1, 01.03.2002, p. 8-13.

Research output: Contribution to journalArticle

Saeki, Hiroshi ; Oda, Shinya ; Kawaguchi, Hidetoshi ; Ohno, Shinji ; Kuwano, Hiroyuki ; Maehara, Yoshihiko ; Sugimachi, Keizo. / Concurrent overexpression of Ets-1 and c-Met correlates with a phenotype of high cellular motility in human esophageal cancer. In: International Journal of Cancer. 2002 ; Vol. 98, No. 1. pp. 8-13.
@article{d807db366e2c43b28905d0891269e8d5,
title = "Concurrent overexpression of Ets-1 and c-Met correlates with a phenotype of high cellular motility in human esophageal cancer",
abstract = "Hepatocyte growth factor (HGF) stimulates cell motility as well as mitotic activity of cells. High concentrations of HGF or overexpression of its cellular receptor c-Met in cancer have been reported. We analyzed the expression status of c-Met immunohistochemically in 76 cases of human esophageal cancer. Overexpression of c-Met was noted at a considerably high frequency. Intriguingly, c-Met overexpression was frequent in a specific type of cell nest formation in tumors, i.e., the small nest type, in which tumors form small, dispersed cell nests. Further immunohistochemical analyses using serial sections revealed a striking coincidence between overexpression of c-Met and its transcriptional factor, Ets-1. Overexpression of c-Met and Ets-1 was statistically more frequent in small nest type tumors. The close correlation in expression status between Ets-1 and c-Met was also confirmed using 6 established human esophageal cancer cell lines. In addition, cells that expressed high levels of Ets-1 and c-Met exhibited an extremely motile phenotype by HGF stimulation in vitro. The presence of HGF in tissue sections was confirmed using similar immunohistochemical approaches. These observations suggest that in human esophageal cancer cells the transcriptional factor Ets-1 upregulates the expression of c-Met and, consequently, confers on cells a highly motile phenotype leading to a specific form of tumor development.",
author = "Hiroshi Saeki and Shinya Oda and Hidetoshi Kawaguchi and Shinji Ohno and Hiroyuki Kuwano and Yoshihiko Maehara and Keizo Sugimachi",
year = "2002",
month = "3",
day = "1",
doi = "10.1002/ijc.10163",
language = "English",
volume = "98",
pages = "8--13",
journal = "International Journal of Cancer",
issn = "0020-7136",
publisher = "Wiley-Liss Inc.",
number = "1",

}

TY - JOUR

T1 - Concurrent overexpression of Ets-1 and c-Met correlates with a phenotype of high cellular motility in human esophageal cancer

AU - Saeki, Hiroshi

AU - Oda, Shinya

AU - Kawaguchi, Hidetoshi

AU - Ohno, Shinji

AU - Kuwano, Hiroyuki

AU - Maehara, Yoshihiko

AU - Sugimachi, Keizo

PY - 2002/3/1

Y1 - 2002/3/1

N2 - Hepatocyte growth factor (HGF) stimulates cell motility as well as mitotic activity of cells. High concentrations of HGF or overexpression of its cellular receptor c-Met in cancer have been reported. We analyzed the expression status of c-Met immunohistochemically in 76 cases of human esophageal cancer. Overexpression of c-Met was noted at a considerably high frequency. Intriguingly, c-Met overexpression was frequent in a specific type of cell nest formation in tumors, i.e., the small nest type, in which tumors form small, dispersed cell nests. Further immunohistochemical analyses using serial sections revealed a striking coincidence between overexpression of c-Met and its transcriptional factor, Ets-1. Overexpression of c-Met and Ets-1 was statistically more frequent in small nest type tumors. The close correlation in expression status between Ets-1 and c-Met was also confirmed using 6 established human esophageal cancer cell lines. In addition, cells that expressed high levels of Ets-1 and c-Met exhibited an extremely motile phenotype by HGF stimulation in vitro. The presence of HGF in tissue sections was confirmed using similar immunohistochemical approaches. These observations suggest that in human esophageal cancer cells the transcriptional factor Ets-1 upregulates the expression of c-Met and, consequently, confers on cells a highly motile phenotype leading to a specific form of tumor development.

AB - Hepatocyte growth factor (HGF) stimulates cell motility as well as mitotic activity of cells. High concentrations of HGF or overexpression of its cellular receptor c-Met in cancer have been reported. We analyzed the expression status of c-Met immunohistochemically in 76 cases of human esophageal cancer. Overexpression of c-Met was noted at a considerably high frequency. Intriguingly, c-Met overexpression was frequent in a specific type of cell nest formation in tumors, i.e., the small nest type, in which tumors form small, dispersed cell nests. Further immunohistochemical analyses using serial sections revealed a striking coincidence between overexpression of c-Met and its transcriptional factor, Ets-1. Overexpression of c-Met and Ets-1 was statistically more frequent in small nest type tumors. The close correlation in expression status between Ets-1 and c-Met was also confirmed using 6 established human esophageal cancer cell lines. In addition, cells that expressed high levels of Ets-1 and c-Met exhibited an extremely motile phenotype by HGF stimulation in vitro. The presence of HGF in tissue sections was confirmed using similar immunohistochemical approaches. These observations suggest that in human esophageal cancer cells the transcriptional factor Ets-1 upregulates the expression of c-Met and, consequently, confers on cells a highly motile phenotype leading to a specific form of tumor development.

UR - http://www.scopus.com/inward/record.url?scp=0036497903&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036497903&partnerID=8YFLogxK

U2 - 10.1002/ijc.10163

DO - 10.1002/ijc.10163

M3 - Article

C2 - 11857377

AN - SCOPUS:0036497903

VL - 98

SP - 8

EP - 13

JO - International Journal of Cancer

JF - International Journal of Cancer

SN - 0020-7136

IS - 1

ER -