MEK-ERK-dependent multiple caspase activation by mitochondrial proapoptotic Bcl-2 family proteins is essential for heavy ion irradiation-induced glioma cell death.
作者： A Tomiyama , K Tachibana , K Suzuki , S Seino , J Sunayama
关键词: Caspase 、 Caspase 8 、 Cancer research 、 Apoptosis 、 Protein kinase A 、 MAPK/ERK pathway 、 Biology 、 Bcl-2-associated X protein 、 Glioma 、 Cell biology 、 Mitogen-activated protein kinase kinase
摘要: Recently developed heavy ion irradiation therapy using a carbon beam (CB) against systemic malignancy has numerous advantages. However, the clinical results of CB glioblastoma still have room for improvement. Therefore, we tried to clarify molecular mechanism CB-induced glioma cell death. T98G and U251 human lines were irradiated by CB, caspase-dependent apoptosis was induced in both dose-dependent manner. Knockdown Bax (BCL-2-associated X protein) Bak killer) overexpression Bcl-2 or Bcl-xl (B-cell lymphoma-extra large) showed involvement family proteins upstream caspase activation, including caspase-8, We also detected activation extracellular signal-regulated kinase (ERK) knockdown ERK regulator mitogen-activated protein (MEK)1/2 dominant-negative (DN) inhibited death mitochondria. In addition, application MEK-specific inhibitors defined periods that recovery between 2 36 h after is essential Furthermore, MEK DN failed significantly inhibit X-ray-induced These suggested MEK–ERK cascade crucial role death, which known limited contribution
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