Nitidine chloride inhibits renal cancer cell metastasis via suppressing AKT signaling pathway.

Abstract

Nitidine Chloride (NC) has been shown to have anti-cancer effects on various tumors. However, whether NC could exert anti-metastasis activity in renal cancer cells and the underlying mechanisms have not been elucidated. In this work, our data demonstrated the anti-metastasis effects of NC on renal cancer cells in vitro. With scratch assay and transwell assays, we found that NC potently suppressed the migration and invasion of 786-O and A498 cells. Mechanistically, we presented that NC significantly decreased phosphorylation of AKT, accompanied by down-regulation of MMP-2 and MMP-9. Furthermore, a specific AKT inhibitor, LY294002, could enhance the anti-metastasis effects of NC, which indicated that NC suppressed metastasis of renal cancer cells partly via inhibition of AKT activity. Taken together, our results imply that NC can be developed as a potential anti-metastasis agent to renal cancer.

• Authors: Zhiqing Fang, Yueqing Tang, Wei Jiao, Zhaoquan Xing, Zhaoxin Guo, Weichang Wang, Benkang Shi, Zhonghua Xu, Zhaoxu Liu
• Journal: Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association (Food Chem Toxicol) Vol. 60 Pg. 246-51 (Oct 2013) ISSN: 1873-6351 [Electronic] England
• PMID: 23911800 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2013 Elsevier Ltd. All rights reserved.

Chemical References

• Antineoplastic Agents
• Benzophenanthridines
• nitidine
• Proto-Oncogene Proteins c-akt
• MMP2 protein, human
• Matrix Metalloproteinase 2
• MMP9 protein, human
• Matrix Metalloproteinase 9

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Benzophenanthridines (pharmacology)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cell Survival (drug effects)
• Down-Regulation
• Humans
• Kidney Neoplasms (metabolism, pathology)
• Matrix Metalloproteinase 2 (genetics, metabolism)
• Matrix Metalloproteinase 9 (genetics, metabolism)
• Neoplasm Metastasis
• Phosphorylation
• Proto-Oncogene Proteins c-akt (genetics, metabolism)
• Signal Transduction (drug effects)