Differential regulation of the antiapoptotic action of B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma extra long (Bcl-xL) by c-Jun N-terminal protein kinase (JNK) 1-involved pathway in neuroglioma cells.

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.

• 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)

Chemical References

• Antineoplastic Agents, Phytogenic
• Apoptosis Regulatory Proteins
• Proto-Oncogene Proteins c-bcl-2
• bcl-X Protein
• Etoposide
• Mitogen-Activated Protein Kinase 8

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)