Activated Ki-ras enhances sensitivity of ceramide-induced apoptosis without c-Jun NH2-terminal kinase/stress-activated protein kinase or extracellular signal-regulated kinase activation in human colon cancer cells

Mariko Ohmori, Senji Shirasawa, Masanori Furuse, Koji Okumura, Takehiko Sasazuki

研究成果: Contribution to journalArticle査読

23 被引用数 (Scopus)

抄録

The activation of c-Jun NH2-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and/or extracellular signal-regulated kinase (ERK) is involved in ceramide-induced apoptosis in certain cells. To examine the relationship between activated Ki-ras-mediated signals and ceramide-induced apoptosis in human colon cancer cells, JNK/SAPK and ERK activity, as initiated by ceramide, was examined in HCT116, which has a mutation of Ki- ras at codon 13, and HCT116-derived clones, HKe-3 and HKh-2, in which activated Ki-ras was disrupted through gene targeting. In HKe-3 and HKh-2, the activity of JNK/SAPK increased significantly within 60 min following C2 ceramide stimulation, and some apoptosis followed. In contrast, C2 ceramide caused a marked apoptosis in HCT116, but activation of JNK/SAPK was not observed. C2 ceramide did not activate ERK in any of the cell lines. These results suggest that activated Ki-ras contributes to the sensitivity of ceramide-induced apoptosis without JNK/SAPK or ERK activation and that other signaling pathways involved in ceramide-induced apoptosis may be present in human colon cancer cells.

本文言語英語
ページ(範囲)4714-4717
ページ数4
ジャーナルCancer Research
57
21
出版ステータス出版済み - 11 1 1997

All Science Journal Classification (ASJC) codes

  • 癌研究
  • 腫瘍学

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