Targeting cathepsin S induces tumor cell autophagy via the EGFR–ERK signaling pathway
Copyright policy )Targeting cathepsin S induces tumor cell autophagy via the EGFR–ERK signaling pathway
Cathepsin S is a cellular cysteine protease, which is frequently over-expressed in human cancer cells and plays important role in tumor metastasis. However, the role of cathepsin S in regulating cancer cell survival and death remains undefined. The aim of this study was to determine whether targeting cathepsin S could induce autophagy/apoptosis in cancer cells. In this study, we demonstrated that targeting cathepsin S by either specific small molecular inhibitors or cathepsin S siRNA induced autophagy and subsequent apoptosis in human cancer cells, and the induction of autophagy was dependent on the phosphorylation of EGFR and activation of the EGFR-related ERK/MAPK-signaling pathway. In conclusion, the current study reveals that cathepsin S plays an important role in the regulation of cell autophagy through interference with the EGFR-ERK/MAPK-signaling pathway.
Time Factors, Dose-Response Relationship, Drug, Antineoplastic Agents, CHO Cells, Cathepsins, Enzyme Activation, ErbB Receptors, Cricetulus, Cricetinae, Neoplasms, Autophagy, Animals, Humans, RNA Interference, Molecular Targeted Therapy, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, HT29 Cells, Protein Kinase Inhibitors, Signal Transduction
Time Factors, Dose-Response Relationship, Drug, Antineoplastic Agents, CHO Cells, Cathepsins, Enzyme Activation, ErbB Receptors, Cricetulus, Cricetinae, Neoplasms, Autophagy, Animals, Humans, RNA Interference, Molecular Targeted Therapy, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, HT29 Cells, Protein Kinase Inhibitors, Signal Transduction
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