Activation of MAPK pathways and downstream transcription factors in 2-aminobiphenyl-induced apoptosis

Lei Chin Chen, Tsung Cheng Chueh, Yen Fan Tuan, Chien Cheng Chen, Chih Ching Chien, Huey Yin Lee, Ssu Ching Chen

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


2-Aminobiphenyls (2-ABP) induces oxidative DNA damage and leads to apoptosis. The precise signaling pathways of inducing apoptosis in vitro are still unknown. This study provides insight into the relationship between 2-ABP-induced apoptosis and the activation of MAPK and downstream transcription factors using pharmacological inhibitors of ERK, p38, and JNK pathways. Results showed that 2-ABP induced the activation of ERK and JNK but not p38. The ERK/JNK pathways downstream transcription factors, c-Jun and ATF-2, were also activated by 2-ABP. The inhibitory effects of ERK inhibitor, U0126, on 2-ABP-induced caspase-3 activity were not detected. However, JNK inhibitor, SP600125, significantly attenuated the caspase-3 activity induced by 2-ABP. The expression of the transcription factors c-Jun and ATF-2 were decreased in 2-ABP treated cells in the presence of ERK/JNK inhibitors, suggesting that the expression of ERK/JNK pathways leads to the downstream activation of c-Jun and ATF-2. N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade.

Original languageEnglish
Pages (from-to)205-211
Number of pages7
JournalEnvironmental Toxicology
Issue number2
StatePublished - 1 Feb 2015


  • 2-aminobiphenyl
  • ATF-2
  • C-Jun
  • Caspase-3
  • ERK
  • JNK
  • N-acetylcysteine


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