転写因子NF-κBの制御に基づいた口腔癌治療  [in Japanese] THERAPY OF PATIENTS WITH ORAL CANCER BASED ON THE REGULATION OF A TRANSCRIPTION FACTOR, NF-κB  [in Japanese]

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Author(s)

    • 東 雅之 AZUMA Masayuki
    • 徳島大学歯学部口腔外科学第二講座 Second Department of Oral and Maxillofacial Surgery, Tokushima University School of Dentistry
    • 佐藤 光信 SATO Mitsunobu
    • 徳島大学歯学部口腔外科学第二講座 Second Department of Oral and Maxillofacial Surgery, Tokushima University School of Dentistry

Abstract

口腔癌細胞へのNF-κBの構成的抑制因子である変異型IκB-α cDNAの導入により, 口腔癌細胞はヌードマウスでの腫瘍原性において著しい低下を示した。この造腫瘍性の低下は遺伝子導入癌細胞からのIL-1α, IL-6, IL-8, VEGF産生の抑制に起因していることが示唆された。一方, 口腔癌細胞は放射線や5-FUによりIL-6やIL-8の明らかな産生誘導が認められたが, 遺伝子導入癌細胞においてはそれらの産生誘導の有意な抑制がみられた。したがって, 変異型IκB-α cDNAの導入は口腔癌細胞の腫瘍原性を低下させるのみならず, 放射線や抗癌剤に対する感受性を増強させることが確認された。以上の結果より, NF-κBの抑制は口腔癌治療の成績向上に寄与する可能性が示唆された。

We found that the tumor-forming ability in nude mice of the super-repressor form of IκBα (srIκBα) cDNA-transfected human oral squamous carcinoma cell (B88) clones (B88mI-1, -2, and -3) was significantly lower than that of B88 or empty vector-transfected cell clones (B88neo). This suppressed ability in tumorigenicity was attributed to the remarkable down-regulation of the expression of IL-1α, IL-6, IL-8, and VEGF in B88mI cell clones as compared to that in B88 or B88neo. When tumor-bearing nude mice were treated with ionizing radiation (IR) or 5-FU, the suppression of tumor growth was significantly augmented in B88mI cell clones as compared to that in B88 or B88neo. ELISA analysis indicated that although a remarkable increase in production of IL-6 and IL-8 was observed in B88 and B88neo after <i>in vitro</i> exposure to IR or treatment with 5-FU, radio- and chemotherapy-induced production of these cytokines was significantly suppressed in B88mI cell clones.

Journal

  • Japanese jornal of Head and Neck Cancer

    Japanese jornal of Head and Neck Cancer 29(3), 493-498, 2003-09-25

    Japan Society for Head and Neck Cancer

References:  14

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