Jeong Hyo-Soon, Choi Hye-Yeon, Choi Tae-Won, Kim Bong-Woo, Kim Jung-Hyun, Lee Eung-Ryoung, Cho Ssang-Goo
Department of Animal Biotechnology, Konkuk University, Seoul, Korea.
Biol Pharm Bull. 2008 Sep;31(9):1686-90. doi: 10.1248/bpb.31.1686.
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.
在此，我们证实，N18TG神经胶质瘤细胞中B细胞淋巴瘤-XL（Bcl-xL）的稳定表达可抑制依托泊苷处理引起的c-Jun氨基末端蛋白激酶（JNK）激活、核碎裂和细胞死亡。此外，JNK1的额外过表达导致部分拮抗Bcl-xL所营造的抗凋亡环境，这意味着JNK1相关途径可能在下调Bcl-xL的抗凋亡作用中发挥作用。然而，JNK1对Bcl-xL抗凋亡作用的拮抗作用明显弱于其对Bcl-2作用的拮抗作用。有趣的是，我们发现JNK1的过表达导致Bcl-xL表达增加。因此，这些结果表明，Bcl-xL和Bcl-2可能通过不同机制诱导其抗凋亡作用，提示JNK1相关途径可能参与Bcl-xL的表达。
