MIG-7 controls COX-2/PGE2-mediated lung cancer metastasis.

Ming-Yi Ho, Shu-Mei Liang, Shao-Wen Hung, Chi-Ming Liang
Author Information
  1. Ming-Yi Ho: Genomics Research Center, Academia Sinica, Taipei, Taiwan, ROC.

Abstract

More effective treatments for metastatic lung cancer remain a pressing clinical need. In this study, we identified migration inducting gene-7 (MIG-7) protein as critical for COX-2/prostaglandin E2 (PGE2)- and Akt/GSK-3β-dependent tumor invasion/metastasis. COX-2/PGE2 activated EP4 to enhance Akt and GSK-3β phosphorylation and β-catenin/T-cell factor/lymphoid enhancer factor signaling leading to MIG-7 upregulation. RNAi-mediated attenuation of MIG-7 blocked COX-2/PGE2- and Akt/GSK-3β-mediated migration/invasion effects. Furthermore, MIG-7 protein inhibited protein phosphatase 2A to sustain Akt/GSK-3β phosphorylation and cancer-cell migration/invasion. Cancer cells overexpressing MIG-7 exhibited increased expression of ZEB-1 and Twist in parallel with epithelial-mesenchymal transition, metastasis and cancer lethality. MIG-7 protein level positively correlated with advanced stages of human lung cancers. MIG-7 thus offers a theranostic target for cancer metastases arising from aberrant activation of the cellular COX-2/PGE2 and Akt/GSK-3β signaling pathways.

MeSH Term

Animals
Cell Movement
Cyclooxygenase 2
Dinoprostone
Epithelial-Mesenchymal Transition
Humans
Immunoblotting
Immunohistochemistry
Immunoprecipitation
Lung Neoplasms
Male
Mice
Mice, SCID
Neoplasm Invasiveness
Neoplasm Proteins
Signal Transduction
Tissue Array Analysis

Chemicals

Neoplasm Proteins
TOX4 protein, human
Cyclooxygenase 2
Dinoprostone

Word Cloud

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