ヒト未分化大細胞性リンパ腫由来Ki-JK細胞に対するCD30の抗アポトーシス作用

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  • ヒト ミブンカ ダイ サイボウセイ リンパシュ ユライ Ki-JK サイボウ ニ タイスル CD30 ノ コウアポトーシス サヨウ
  • CD30 Triggered Anti-apoptosis in Anaplastic Large Cell Lymphoma Cells

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Human CD30^+ anaplastic large cell lymphoma (ALCL) demonstrates kinase activity of p80^<NPM/ALK> protein. Protein kinase activities are important in regulating the biological activities of cells. In this report we investigated the response to anti-CD30 antibody (aCD30Ab) plus protein kinase inhibitors (ML-9, A-3, H-7 and sphingosine) in CD30^+ ALCL Ki-JK cells. All protein kinase inhibitors alone and aCD30Ab alone induced apoptosis, but aCD30Ab prevented ML-9-induced apoptosis in Ki-JK cells, and interleukin (IL)-8 was produced only when the combination of aCD30Ab plus ML-9 was applied. Human recombinant IL-8 and the IL-8 antisense oligonucleotide prevented ML-9-induced apoptosis, the IL-8 was related to the aCD30Ab-induced anti-apoptosis effect. The aCD30Ab-induced anti-apoptotic effect was associated with activation of nuclear factor kappa B (NF-κB). Exogenous addition of IL-8 increased anti-apoptotic protein bcl-2. In anti-apoptosis of CD30 triggering, activated NF-κB produced IL-8, then IL-8 augmented bcl-2 protein. ML-9 suppressed NPM/ALK expression incompletely. These results data suggest that aCD30Ab had apoptotic and anti-apoptotic effects. Anti-apoptosis was mediated by NF-κB activation and IL-8 production. The ML-9-induced apoptosis effect was associated with suppression of NPM/ALK. This study indicated the effects and risks of aCD30Ab alone or in combination with the protein kinase inhibitors in CD30^+ ALCL cells.

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