Analysis of Fas and Fas ligand expression and function in lung cancer cell lines

M. Kawasaki, K. Kuwano, Y. Nakanishi, N. Hagimoto, K. Takayama, Xin-Hai Pei, T. Maeyama, M. Yoshimi, N. Hara

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

The aim of this study was to investigate the expression of Fas and Fas ligand (FasL) and to determine the significance of these molecules in lung cancer cell lines. Immunoblotting, RT-PCR and flow cytometric analyses were carried out to measure the expression of Fas and FasL and to examine their interactions and effects on cell growth and apoptosis. Fas and FasL were co-expressed in most of the cell lines but to varying degrees. Apoptosis induced by the agonistic anti-Fas antibody was significantly correlated with Fas expression (P=0.0075), whereas cisplatin-induced apoptosis was not. Upregulation of Fas and FasL expression by the administration of cisplatin was found in 7 of 11 (64%) and 9 of 11 (82%) cell lines, respectively. However, cisplatin-induced apoptosis was not suppressed by antagonistic anti-FasL antibody. Thus, our data indicated that Fas and FasL were co-expressed in lung cancer cell lines, and that Fas ligation induced by agonistic anti-Fas antibody is functional and induced apoptosis that was dependent on the levels of Fas expression. In contrast, Fas-FasL interactions appeared to be non-functional. Furthermore, our results suggest that cisplatin-induced apoptosis in lung cancer cells was independent of the Fas-FasL interaction. Copyright (C) 2000 Elsevier Science Ltd.

Original languageEnglish (US)
Pages (from-to)656-663
Number of pages8
JournalEuropean Journal of Cancer
Volume36
Issue number5
DOIs
StatePublished - Mar 2000
Externally publishedYes

Fingerprint

Fas Ligand Protein
Lung Neoplasms
Cell Line
Apoptosis
Cisplatin
Anti-Idiotypic Antibodies
Immunoblotting
Ligation
Up-Regulation
Polymerase Chain Reaction
Antibodies
Growth

Keywords

  • Apoptosis
  • Cisplatin
  • Fas
  • Fas ligand
  • Lung cancer

ASJC Scopus subject areas

  • Cancer Research
  • Hematology
  • Oncology

Cite this

Kawasaki, M., Kuwano, K., Nakanishi, Y., Hagimoto, N., Takayama, K., Pei, X-H., ... Hara, N. (2000). Analysis of Fas and Fas ligand expression and function in lung cancer cell lines. European Journal of Cancer, 36(5), 656-663. https://doi.org/10.1016/S0959-8049(99)00332-9

Analysis of Fas and Fas ligand expression and function in lung cancer cell lines. / Kawasaki, M.; Kuwano, K.; Nakanishi, Y.; Hagimoto, N.; Takayama, K.; Pei, Xin-Hai; Maeyama, T.; Yoshimi, M.; Hara, N.

In: European Journal of Cancer, Vol. 36, No. 5, 03.2000, p. 656-663.

Research output: Contribution to journalArticle

Kawasaki, M, Kuwano, K, Nakanishi, Y, Hagimoto, N, Takayama, K, Pei, X-H, Maeyama, T, Yoshimi, M & Hara, N 2000, 'Analysis of Fas and Fas ligand expression and function in lung cancer cell lines', European Journal of Cancer, vol. 36, no. 5, pp. 656-663. https://doi.org/10.1016/S0959-8049(99)00332-9
Kawasaki, M. ; Kuwano, K. ; Nakanishi, Y. ; Hagimoto, N. ; Takayama, K. ; Pei, Xin-Hai ; Maeyama, T. ; Yoshimi, M. ; Hara, N. / Analysis of Fas and Fas ligand expression and function in lung cancer cell lines. In: European Journal of Cancer. 2000 ; Vol. 36, No. 5. pp. 656-663.
@article{3ca5d8125a9e4f7691cbb7782e28092e,
title = "Analysis of Fas and Fas ligand expression and function in lung cancer cell lines",
abstract = "The aim of this study was to investigate the expression of Fas and Fas ligand (FasL) and to determine the significance of these molecules in lung cancer cell lines. Immunoblotting, RT-PCR and flow cytometric analyses were carried out to measure the expression of Fas and FasL and to examine their interactions and effects on cell growth and apoptosis. Fas and FasL were co-expressed in most of the cell lines but to varying degrees. Apoptosis induced by the agonistic anti-Fas antibody was significantly correlated with Fas expression (P=0.0075), whereas cisplatin-induced apoptosis was not. Upregulation of Fas and FasL expression by the administration of cisplatin was found in 7 of 11 (64{\%}) and 9 of 11 (82{\%}) cell lines, respectively. However, cisplatin-induced apoptosis was not suppressed by antagonistic anti-FasL antibody. Thus, our data indicated that Fas and FasL were co-expressed in lung cancer cell lines, and that Fas ligation induced by agonistic anti-Fas antibody is functional and induced apoptosis that was dependent on the levels of Fas expression. In contrast, Fas-FasL interactions appeared to be non-functional. Furthermore, our results suggest that cisplatin-induced apoptosis in lung cancer cells was independent of the Fas-FasL interaction. Copyright (C) 2000 Elsevier Science Ltd.",
keywords = "Apoptosis, Cisplatin, Fas, Fas ligand, Lung cancer",
author = "M. Kawasaki and K. Kuwano and Y. Nakanishi and N. Hagimoto and K. Takayama and Xin-Hai Pei and T. Maeyama and M. Yoshimi and N. Hara",
year = "2000",
month = "3",
doi = "10.1016/S0959-8049(99)00332-9",
language = "English (US)",
volume = "36",
pages = "656--663",
journal = "European Journal of Cancer",
issn = "0959-8049",
publisher = "Elsevier Limited",
number = "5",

}

TY - JOUR

T1 - Analysis of Fas and Fas ligand expression and function in lung cancer cell lines

AU - Kawasaki, M.

AU - Kuwano, K.

AU - Nakanishi, Y.

AU - Hagimoto, N.

AU - Takayama, K.

AU - Pei, Xin-Hai

AU - Maeyama, T.

AU - Yoshimi, M.

AU - Hara, N.

PY - 2000/3

Y1 - 2000/3

N2 - The aim of this study was to investigate the expression of Fas and Fas ligand (FasL) and to determine the significance of these molecules in lung cancer cell lines. Immunoblotting, RT-PCR and flow cytometric analyses were carried out to measure the expression of Fas and FasL and to examine their interactions and effects on cell growth and apoptosis. Fas and FasL were co-expressed in most of the cell lines but to varying degrees. Apoptosis induced by the agonistic anti-Fas antibody was significantly correlated with Fas expression (P=0.0075), whereas cisplatin-induced apoptosis was not. Upregulation of Fas and FasL expression by the administration of cisplatin was found in 7 of 11 (64%) and 9 of 11 (82%) cell lines, respectively. However, cisplatin-induced apoptosis was not suppressed by antagonistic anti-FasL antibody. Thus, our data indicated that Fas and FasL were co-expressed in lung cancer cell lines, and that Fas ligation induced by agonistic anti-Fas antibody is functional and induced apoptosis that was dependent on the levels of Fas expression. In contrast, Fas-FasL interactions appeared to be non-functional. Furthermore, our results suggest that cisplatin-induced apoptosis in lung cancer cells was independent of the Fas-FasL interaction. Copyright (C) 2000 Elsevier Science Ltd.

AB - The aim of this study was to investigate the expression of Fas and Fas ligand (FasL) and to determine the significance of these molecules in lung cancer cell lines. Immunoblotting, RT-PCR and flow cytometric analyses were carried out to measure the expression of Fas and FasL and to examine their interactions and effects on cell growth and apoptosis. Fas and FasL were co-expressed in most of the cell lines but to varying degrees. Apoptosis induced by the agonistic anti-Fas antibody was significantly correlated with Fas expression (P=0.0075), whereas cisplatin-induced apoptosis was not. Upregulation of Fas and FasL expression by the administration of cisplatin was found in 7 of 11 (64%) and 9 of 11 (82%) cell lines, respectively. However, cisplatin-induced apoptosis was not suppressed by antagonistic anti-FasL antibody. Thus, our data indicated that Fas and FasL were co-expressed in lung cancer cell lines, and that Fas ligation induced by agonistic anti-Fas antibody is functional and induced apoptosis that was dependent on the levels of Fas expression. In contrast, Fas-FasL interactions appeared to be non-functional. Furthermore, our results suggest that cisplatin-induced apoptosis in lung cancer cells was independent of the Fas-FasL interaction. Copyright (C) 2000 Elsevier Science Ltd.

KW - Apoptosis

KW - Cisplatin

KW - Fas

KW - Fas ligand

KW - Lung cancer

UR - http://www.scopus.com/inward/record.url?scp=0034100464&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034100464&partnerID=8YFLogxK

U2 - 10.1016/S0959-8049(99)00332-9

DO - 10.1016/S0959-8049(99)00332-9

M3 - Article

C2 - 10738132

AN - SCOPUS:0034100464

VL - 36

SP - 656

EP - 663

JO - European Journal of Cancer

JF - European Journal of Cancer

SN - 0959-8049

IS - 5

ER -