Curcumin suppresses proliferation and invasion in non-small cell lung cancer by modulation of MTA1-mediated Wnt/β-catenin pathway.

Abstract

Curcumin, a naturally occurring phenolic compound, has a diversity of antitumor activities. It has been previously demonstrated that curcumin can inhibit the invasion and metastasis of tumors through activation of the tumor suppressor DnaJ-like heat shock protein 40 (HLJ1). However, the specific roles and mechanisms of curcumin in regulating the malignant behaviors of non-small cell lung cancer (NSCLC) cells still remain unclear. In this study, we found that curcumin could inhibit the proliferation and invasion of NSCLC cells and induce G0/G1 phase arrest. Metastasis-associated protein 1 (MTA1) overexpression has been detected in a wide variety of aggressive tumors and plays an important role on cell invasion and metastasis. Our results showed that curcumin could effectively inhibit the MTA1 expression of NSCLC cells. Further research on the subsequent mechanism showed that curcumin inhibited the proliferation and invasion of NSCLC cells through MTA1-mediated inactivation of Wnt/β-catenin pathway. Wnt/β-catenin signaling was reported to play a critical cooperative role on promoting lung tumorigenesis. Thus, these investigations provided novel insights into the mechanisms of curcumin on inhibition of NSCLC cell growth and invasion and showed potential therapeutic strategies for NSCLC.

• Authors: Yimin Lu, Changjiang Wei, Zhaoqing Xi
• Journal: In vitro cellular & developmental biology. Animal (In Vitro Cell Dev Biol Anim) Vol. 50 Issue 9 Pg. 840-50 (Oct 2014) ISSN: 1543-706X [Electronic] Germany
• PMID: 24938356 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• Mta1 protein, human
• Repressor Proteins
• Trans-Activators
• Histone Deacetylases
• Curcumin

Topics

• Antineoplastic Agents (pharmacology)
• Carcinoma, Non-Small-Cell Lung (pathology)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Curcumin (pharmacology)
• G1 Phase Cell Cycle Checkpoints
• Gene Expression Regulation, Neoplastic (drug effects)
• Histone Deacetylases (genetics, metabolism)
• Humans
• Neoplasm Invasiveness
• Repressor Proteins (genetics, metabolism)
• Trans-Activators
• Wnt Signaling Pathway (drug effects)