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The pivotal role of c-Jun NH2-terminal kinase-mediated Beclin 1 expression during anticancer agents-induced autophagy in cancer cells
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The pivotal role of c-Jun NH2-terminal kinase-mediated Beclin 1 expression during anticancer agents-induced autophagy in cancer cells
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Journal Article
The pivotal role of c-Jun NH2-terminal kinase-mediated Beclin 1 expression during anticancer agents-induced autophagy in cancer cells
2009
Overview
The c-Jun NH2-terminal kinase (JNK) pathway represents one subgroup of MAP kinases that are activated primarily by cytokines and exposure to environmental stress. Autophagy is a protein-degradation system characterized by the formation of double-membrane vacuoles termed autophagosomes. Autophagy-related gene
beclin 1
plays a key role in autophagosome formation. However, the relationships between activation of JNK pathway, autophagy induction and Beclin 1 expression remain elusive. In this study, we used human cancer cell lines CNE2 and Hep3B to investigate the role of JNK-mediated Beclin 1 expression in ceramide-induced autophagic cell death. Ceramide-treated cells exhibited the characteristics of autophagy (that is, acidic vesicular organelle formation and the LC3-II generation). JNK was activated in these two cell lines exposed to ceramide and the phosphorylation of c-Jun also increased. In the meantime, we found that ceramide upregulated Beclin 1 expression in cancer cells. The upregulation of Beclin 1 expression could be blocked by SP600125 (a specific inhibitor of JNK) or a small interfering RNA (siRNA) directed against JNK1/2 or c-Jun. Chromatin immunoprecipitation and luciferase reporter analysis revealed that c-Jun was involved in the regulation of
beclin 1
transcription in response to ceramide treatment. In addition, inhibition of JNK activity by SP600125 could inhibit autophagy induction by ceramide. Furthermore, Beclin 1 knockdown by siRNA also inhibited ceramide-mediated autophagic cell death. JNK-mediated Beclin 1 expression was also observed in topotecan-induced autophagy. These data suggest that activation of JNK pathway can mediate Beclin 1 expression, which plays a key role in autophagic cell death in cancer cells.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Antineoplastic Agents - pharmacology
/ Apoptosis Regulatory Proteins - metabolism
/ Beclin-1
/ Biological and medical sciences
/ Cancer
/ Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
/ Ceramide
/ Enzyme Inhibitors - pharmacology
/ Fundamental and applied biological sciences. Psychology
/ Gene Expression Regulation, Neoplastic
/ Genes
/ Genetics
/ Humans
/ JNK Mitogen-Activated Protein Kinases - metabolism
/ Kinases
/ MAP Kinase Kinase 4 - metabolism
/ Medicine
/ Membrane Proteins - metabolism
/ Molecular and cellular biology
/ Oncology
/ RNA, Small Interfering - metabolism
/ siRNA
/ Vacuoles
