Abstract |
Here, we confirmed that stable expression of B-cell lymphoma-xL (Bcl-xL) in N18TG neuroglioma cells could suppress c-Jun N-terminal protein kinase (JNK) activation, nuclear fragmentation, and cell death caused by etoposide treatment. Moreover, additional overexpression of JNK1 led to partially antagonize the antiapoptotic environment attained by Bcl-xL, implying that JNK1-involved pathway may play a role in down-regulation of the antiapoptotic effect of Bcl-xL. However, the antagonistic effect of JNK1 on the antiapoptotic action of Bcl-xL was significantly weaker than that on the action of Bcl-2. Interestingly, we found that overexpression of JNK1 led to increase of Bcl-xL expression. Thus, these results suggest that Bcl-xL and Bcl-2 may induce its antiapoptotic effect in a different mechanism, provoking the possibility of involvement of JNK1-involved pathway in Bcl-xL expression.
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Authors | Hyo-Soon Jeong, Hye-Yeon Choi, Tae-Won Choi, Bong-Woo Kim, Jung-Hyun Kim, Eung-Ryoung Lee, Ssang-Goo Cho |
Journal | Biological & pharmaceutical bulletin
(Biol Pharm Bull)
Vol. 31
Issue 9
Pg. 1686-90
(Sep 2008)
ISSN: 0918-6158 [Print] Japan |
PMID | 18758060
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents, Phytogenic
- Apoptosis Regulatory Proteins
- Proto-Oncogene Proteins c-bcl-2
- bcl-X Protein
- Etoposide
- Mitogen-Activated Protein Kinase 8
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Topics |
- Antineoplastic Agents, Phytogenic
(pharmacology)
- Apoptosis Regulatory Proteins
(physiology)
- Blotting, Western
- Brain Neoplasms
(metabolism)
- Cell Death
(drug effects)
- Cell Line, Tumor
- Cell Survival
(drug effects)
- DNA Fragmentation
(drug effects)
- Enzyme Activation
(drug effects)
- Etoposide
(pharmacology)
- Glioma
(metabolism)
- Humans
- Mitogen-Activated Protein Kinase 8
(biosynthesis, genetics)
- Proto-Oncogene Proteins c-bcl-2
(biosynthesis, genetics)
- Reverse Transcriptase Polymerase Chain Reaction
- Signal Transduction
(drug effects)
- Transfection
- bcl-X Protein
(biosynthesis, genetics)
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