Necrotic cell death occur via JNK pathway with the activity of transcription factor c-Jun by 4-MC in INS-1 cell line.

Karatug Kacar A. , Bolkent Ş.

Journal of cellular biochemistry, cilt.119, ss.2048-2060, 2018 (SCI Expanded İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 119
  • Basım Tarihi: 2018
  • Doi Numarası: 10.1002/jcb.26367
  • Dergi Adı: Journal of cellular biochemistry
  • Sayfa Sayıları: ss.2048-2060


In this study, it was aimed to determine the doses of 4-methylcatechol causing cell death in rat insulinoma -cells (INS-1), to find out the type of cellular death at these doses, and to investigate the molecular mechanism of cellular death occurring. More necrotic cells were observed than apoptosis with the administration of 350, 400, and 450M 4-methylcatechol. Lactate dehydrogenase levels, reactive oxygen species, mitochondrial potential loss, ATP, and GTP losses increased at these doses. The JNK and ERK cellular pathway were screened. We observed an increase in p-RAF1 activity, the active JNK amount, the total c-Jun amount, while a decrease in p-RAF1 expression, the total JNK amount, JNK expression, ATF2 expression, active ERK, and its expression and Elk1 expression. It was concluded that cells perform necrotic death by the following options: i) phosphorylated RAF1 activates the JNK pathway with the activity of transcription factor c-Jun; ii) Hsp 70 and Hsp 90 do not show a change inside the cell, rendering the JNK pathway active.