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MIG-7 controls COX-2/PGE2-mediated lung cancer metastasis
Ming-Yi Ho1, Shu-Mei Liang, Shao-Wen Hung
1Genomics 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.
Insights
Migration inducting gene-7 (MIG-7) protein drives lung cancer metastasis by promoting tumor invasion. Targeting MIG-7 offers a potential therapeutic strategy for advanced lung cancers.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Metastatic lung cancer requires novel therapeutic targets.
- Tumor invasion and metastasis are complex processes involving multiple signaling pathways.
Purpose of the Study:
- To investigate the role of migration inducting gene-7 (MIG-7) protein in lung cancer metastasis.
- To elucidate the molecular mechanisms by which MIG-7 promotes tumor invasion and metastasis.
- To evaluate MIG-7 as a potential theranostic target.
Main Methods:
- Utilized RNA interference (RNAi) to attenuate MIG-7 expression.
- Investigated the effects of MIG-7 on signaling pathways including COX-2/prostaglandin E2 (PGE2), Akt/GSK-3β, and β-catenin.
- Assessed the impact of MIG-7 on epithelial-mesenchymal transition (EMT), metastasis, and cancer lethality in preclinical models.
- Correlated MIG-7 protein levels with advanced stages in human lung cancer samples.
Main Results:
- MIG-7 protein is critical for COX-2/PGE2- and Akt/GSK-3β-dependent tumor invasion and metastasis.
- COX-2/PGE2 signaling upregulates MIG-7 expression via EP4, Akt/GSK-3β, and β-catenin pathways.
- RNAi-mediated reduction of MIG-7 inhibited cancer cell migration and invasion.
- MIG-7 inhibits protein phosphatase 2A, sustaining Akt/GSK-3β phosphorylation and promoting metastasis.
- Overexpression of MIG-7 correlates with increased ZEB-1, Twist, EMT, metastasis, and lethality.
- MIG-7 protein levels positively correlate with advanced lung cancer stages.
Conclusions:
- MIG-7 protein is a key mediator of lung cancer cell invasion and metastasis.
- The COX-2/PGE2 and Akt/GSK-3β signaling pathways converge on MIG-7 to drive metastatic progression.
- MIG-7 represents a promising theranostic target for managing lung cancer metastasis.
