Clinical Cancer Research CTRC-AACR San Antonio Breast Cancer Symposium
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yamanaka, N.
Right arrow Articles by Katano, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yamanaka, N.
Right arrow Articles by Katano, M.
Clinical Cancer Research Vol. 10, 1853-1859, March 2004
© 2004 American Association for Cancer Research


Cancer Biology

Interleukin 1ß Enhances Invasive Ability of Gastric Carcinoma through Nuclear Factor-{kappa}B Activation

Naoki Yamanaka1, Takashi Morisaki1, Hiroshi Nakashima1, Akira Tasaki1, Makoto Kubo1, Hirotaka Kuga1, Chihiro Nakahara1, Katsuya Nakamura1, Hirokazu Noshiro3, Takashi Yao2, Masazumi Tsuneyoshi2, Masao Tanaka3 and Mitsuo Katano1

Departments of 1 Cancer Therapy and Research, 2 Anatomic Pathology, and 3 Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

Purpose: We examined the role of interleukin (IL)-1ß in activation of nuclear factor {kappa}B (NF-{kappa}B) and the biological function of activated NF-{kappa}B in gastric carcinoma cells.

Experimental Design: Human gastric carcinoma cell line GCTM-1 was used to examine NF-{kappa}B activation by immunostaining and electrophoretic mobility shift assay. Matrix metalloproteinase (MMP)-9 expression, which plays an important role in tumor invasion, was assessed by semiquantitative reverse transcription-PCR, Western blotting, and immunostaining. The invasive ability of GCTM-1 cells was measured by Matrigel invasion assay. In vivo expression of IL-1ß and MMP-9 and activation of NF-{kappa}B in 10 surgically resected gastric carcinoma specimens were examined immunohistochemically.

Results: IL-1ß enhanced NF-{kappa}B activation, MMP-9 expression, and the invasive ability of GCTM-1. A NF-{kappa}B inhibitor, pyrrolidine dithiocarbamate, suppressed both MMP-9 expression and invasiveness of IL-1ß-treated GCTM-1 cells. IL-1ß did not increase the invasive ability of GCTM-1 cells transfected with MMP-9 antisense oligonucleotide. Concomitant expression of IL-1ß and nuclear NF-{kappa}B was observed in 3 of 10 gastric carcinoma specimens. Cells producing IL-1ß were tumor-infiltrating macrophages in two specimens and gastric carcinoma cells in one specimen.

Conclusions: One of the molecules that may play a role in NF-{kappa}B activation in some gastric carcinomas is IL-1ß. The present results suggest that IL-1ß increases the invasive ability of carcinoma cells through activation of NF-{kappa}B and the resulting MMP-9 expression.




This article has been cited by other articles:


Home page
Mol Cancer ResHome page
J. Liu, M. Zhan, J. A.F. Hannay, P. Das, S. V. Bolshakov, D. Kotilingam, D. Yu, A. F. Lazar, R. E. Pollock, and D. Lev
Wild-type p53 Inhibits Nuclear Factor-{kappa}B-Induced Matrix Metalloproteinase-9 Promoter Activation: Implications for Soft Tissue Sarcoma Growth and Metastasis
Mol. Cancer Res., November 1, 2006; 4(11): 803 - 810.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
H. Nakashima, M. Nakamura, H. Yamaguchi, N. Yamanaka, T. Akiyoshi, K. Koga, K. Yamaguchi, M. Tsuneyoshi, M. Tanaka, and M. Katano
Nuclear Factor-{kappa}B Contributes to Hedgehog Signaling Pathway Activation through Sonic Hedgehog Induction in Pancreatic Cancer.
Cancer Res., July 15, 2006; 66(14): 7041 - 7049.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2004 by the American Association for Cancer Research.