ID 250
Title Transcription
テンシャ インシ NF-κB カッセイ ノ ヨクセイ ニヨル コウクウ ヘンペイ ジョウヒガン ノ ホウシャセン カンジュセイ ノ ゾウキョウ
Title Alternative
Enhancement of Radiosensitization in Human Oral Squamous Carcinoma Cells via Suppressing the NF-κB
Author
Motegi, Katsumi Department of Therapeutic Regulation for Oral Tumors, Institute of Health BioSciences, The University of Tokushima Graduate School
Keywords
口腔扁平上皮癌
放射線
NF-κB
アポトーシス
Content Type
Departmental Bulletin Paper
Description
The nuclear factor κB (NF-κB) plays an important role in the development and progression of cancers. We had already reported that NF-κB activity in head and neck carcinoma cells was significantly higher than that in normal oral epithelial cells due to the enhanced phosphorylation and degradation of IκBα protein. We examined the mechanisms underlying the enhancement of radiosensitivity to γ-irradiation (IR) in human oral carcinoma cells (B88) in which NF-κB activity was constitutively suppressed. Super-repressor form of IκBα cDNA-transfected cell clone (B88mI) and empty vector-transfected cell clone (B88neo) was established. We found that the tumor forming ability in nude mice of B88mI clones was significantly lower than that of B88 or B88neo. This suppressed ability in tumorigenicity was attributed to the down regulation of the expression of interleukin (IL)-1 α, IL-6, IL-8 and vascular endothelial growth factor (VEGF) in B88mI cell clones as compared to that in B88 or B88neo. IR induced a much greater degree of apoptosis, as evidenced by flow cytometry analysis and annexin V staining, in B88mI cell clone than B88 or B88neo. When tumor-bearing nude mice were treated with IR, the suppression of tumor growth was significantly augmented in B88mI cell clones as compared to that in B88 or B88neo. These findings indicate that inhibition of NF-κB activity by introducing a super-repressor form of IκBα cDNA into oral cancer cells led to a drastic decrease in tumorigenicity in nude mice and an acquisition of enhanced radiosensitization. Therefore, targeting NF-κB may be a potential approach to controlling the growth of human cancers.
Journal Title
四国歯学会雑誌
ISSN
09146091
NCID
AN10050046
Volume
18
Issue
2
Start Page
179
End Page
185
Sort Key
179
Published Date
2006-01
Remark
公開日:2010年1月24日で登録したコンテンツは、国立情報学研究所において電子化したものです。
EDB ID
FullText File
language
jpn
Report Type
受賞講演