Involvement of NF-κB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma

Yasuo Takamune, Tetsuro Ikebe, Osamu Nagano, Masanori Shinohara

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

The involvement of a disintegrin and metalloprotease domain (ADAM)-17 on the cancer invasion was investigated in oral squamous cell carcinoma (OSCC) cells. TNFα induced the conversion from the proform of ADAM-17 to its mature form time-dependently. TNFα also cleaved CD44 to its small fragments, as observed by a Western blot analysis. The transfection of ADAM-17 siRNA partially suppressed the expression of ADAM-17 as well as the cleavage of CD44. On the other hand, TNFα activated a transcription factor NF-κB in OSCC cells, while NBD peptide, an NF-κB inhibitor, inhibited the ADAM-17 maturation, thus suggesting that NF-κB is involved in ADAM-17 maturation. Moreover, an in vitro invasion assay revealed that both ADAM-17 siRNA and NBD peptides strongly suppressed the TNFα-induced invasion of OSCC cells through the matrix. In conclusion, ADAM-17 plays an important role in cancer invasion probably through CD44 cleavage.

Original languageEnglish
Pages (from-to)393-398
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume365
Issue number2
DOIs
Publication statusPublished - 2008 Jan 11
Externally publishedYes

Fingerprint

Disintegrins
Metalloproteases
Squamous Cell Carcinoma
Small Interfering RNA
Peptides
Epithelial Cells
Transfection
Assays
Neoplasms
Transcription Factors
Western Blotting
Cells

Keywords

  • ADAM-17
  • CD44
  • NF-κB
  • Oral cancer
  • Squamous cell carcinoma
  • TNFα

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Involvement of NF-κB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma. / Takamune, Yasuo; Ikebe, Tetsuro; Nagano, Osamu; Shinohara, Masanori.

In: Biochemical and Biophysical Research Communications, Vol. 365, No. 2, 11.01.2008, p. 393-398.

Research output: Contribution to journalArticle

@article{7260b79cf86d48f4a32f3fecbc503e37,
title = "Involvement of NF-κB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma",
abstract = "The involvement of a disintegrin and metalloprotease domain (ADAM)-17 on the cancer invasion was investigated in oral squamous cell carcinoma (OSCC) cells. TNFα induced the conversion from the proform of ADAM-17 to its mature form time-dependently. TNFα also cleaved CD44 to its small fragments, as observed by a Western blot analysis. The transfection of ADAM-17 siRNA partially suppressed the expression of ADAM-17 as well as the cleavage of CD44. On the other hand, TNFα activated a transcription factor NF-κB in OSCC cells, while NBD peptide, an NF-κB inhibitor, inhibited the ADAM-17 maturation, thus suggesting that NF-κB is involved in ADAM-17 maturation. Moreover, an in vitro invasion assay revealed that both ADAM-17 siRNA and NBD peptides strongly suppressed the TNFα-induced invasion of OSCC cells through the matrix. In conclusion, ADAM-17 plays an important role in cancer invasion probably through CD44 cleavage.",
keywords = "ADAM-17, CD44, NF-κB, Oral cancer, Squamous cell carcinoma, TNFα",
author = "Yasuo Takamune and Tetsuro Ikebe and Osamu Nagano and Masanori Shinohara",
year = "2008",
month = "1",
day = "11",
doi = "10.1016/j.bbrc.2007.11.010",
language = "English",
volume = "365",
pages = "393--398",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Involvement of NF-κB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma

AU - Takamune, Yasuo

AU - Ikebe, Tetsuro

AU - Nagano, Osamu

AU - Shinohara, Masanori

PY - 2008/1/11

Y1 - 2008/1/11

N2 - The involvement of a disintegrin and metalloprotease domain (ADAM)-17 on the cancer invasion was investigated in oral squamous cell carcinoma (OSCC) cells. TNFα induced the conversion from the proform of ADAM-17 to its mature form time-dependently. TNFα also cleaved CD44 to its small fragments, as observed by a Western blot analysis. The transfection of ADAM-17 siRNA partially suppressed the expression of ADAM-17 as well as the cleavage of CD44. On the other hand, TNFα activated a transcription factor NF-κB in OSCC cells, while NBD peptide, an NF-κB inhibitor, inhibited the ADAM-17 maturation, thus suggesting that NF-κB is involved in ADAM-17 maturation. Moreover, an in vitro invasion assay revealed that both ADAM-17 siRNA and NBD peptides strongly suppressed the TNFα-induced invasion of OSCC cells through the matrix. In conclusion, ADAM-17 plays an important role in cancer invasion probably through CD44 cleavage.

AB - The involvement of a disintegrin and metalloprotease domain (ADAM)-17 on the cancer invasion was investigated in oral squamous cell carcinoma (OSCC) cells. TNFα induced the conversion from the proform of ADAM-17 to its mature form time-dependently. TNFα also cleaved CD44 to its small fragments, as observed by a Western blot analysis. The transfection of ADAM-17 siRNA partially suppressed the expression of ADAM-17 as well as the cleavage of CD44. On the other hand, TNFα activated a transcription factor NF-κB in OSCC cells, while NBD peptide, an NF-κB inhibitor, inhibited the ADAM-17 maturation, thus suggesting that NF-κB is involved in ADAM-17 maturation. Moreover, an in vitro invasion assay revealed that both ADAM-17 siRNA and NBD peptides strongly suppressed the TNFα-induced invasion of OSCC cells through the matrix. In conclusion, ADAM-17 plays an important role in cancer invasion probably through CD44 cleavage.

KW - ADAM-17

KW - CD44

KW - NF-κB

KW - Oral cancer

KW - Squamous cell carcinoma

KW - TNFα

UR - http://www.scopus.com/inward/record.url?scp=36248992995&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=36248992995&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2007.11.010

DO - 10.1016/j.bbrc.2007.11.010

M3 - Article

C2 - 17999917

AN - SCOPUS:36248992995

VL - 365

SP - 393

EP - 398

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 2

ER -