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Updated: May 11, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Metastasis suppressor, NDRG1, mediates its activity through signaling pathways and molecular motors
Jing Sun1, Daohai Zhang, Dong-Hun Bae
1Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Abstract:
The metastasis suppressor, N-myc downstream regulated gene 1 (NDRG1), is negatively correlated with tumor progression in multiple neoplasms, being a promising new target for cancer treatment. However, the precise molecular effects of NDRG1 remain unclear. Herein, we summarize recent advances in understanding the impact of NDRG1 on cancer metastasis with emphasis on its interactions with the key oncogenic nuclear factor-kappaB, phosphatidylinositol-3 kinase/phosphorylated AKT/mammalian target of rapamycin and Ras/Raf/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling pathways. Recent studies demonstrating the inhibitory effects of NDRG1 on the epithelial-mesenchymal transition, a key initial step in metastasis, TGF-β pathway and the Wnt/β-catenin pathway are also described. Furthermore, NDRG1 was also demonstrated to regulate molecular motors in cancer cells, leading to inhibition of F-actin polymerization, stress fiber formation and subsequent reduction of cancer cell migration. Collectively, this review summarizes the underlying molecular mechanisms of the antimetastatic effects of NDRG1 in cancer cells.
Insights
N-myc downstream regulated gene 1 (NDRG1) suppresses cancer metastasis by inhibiting key signaling pathways and cellular processes. This review details NDRG1
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- N-myc downstream regulated gene 1 (NDRG1) is a metastasis suppressor implicated in various neoplasms.
- Its precise molecular mechanisms in inhibiting cancer progression remain incompletely understood.
- NDRG1 presents a promising therapeutic target for managing metastatic cancer.
Purpose of the Study:
- To review and synthesize recent findings on NDRG1's role in cancer metastasis.
- To elucidate the molecular mechanisms underlying NDRG1's antimetastatic effects.
- To highlight NDRG1's interactions with critical oncogenic pathways.
Main Methods:
- Literature review of recent studies on NDRG1 and cancer metastasis.
- Analysis of NDRG1's interactions with nuclear factor-kappaB (NF-κB), PI3K/AKT/mTOR, and Ras/Raf/MAPK pathways.
- Examination of NDRG1's effects on epithelial-mesenchymal transition (EMT), TGF-β, and Wnt/β-catenin signaling.
- Investigation of NDRG1's regulation of molecular motors and cytoskeletal dynamics.
Main Results:
- NDRG1 negatively impacts tumor progression and metastasis across multiple cancer types.
- NDRG1 inhibits key oncogenic signaling pathways including NF-κB, PI3K/AKT/mTOR, and Ras/Raf/MAPK.
- NDRG1 suppresses epithelial-mesenchymal transition (EMT), TGF-β, and Wnt/β-catenin pathways.
- NDRG1 regulates molecular motors, inhibiting F-actin polymerization and stress fiber formation, thereby reducing cancer cell migration.
Conclusions:
- NDRG1 exerts potent antimetastatic effects in cancer cells through diverse molecular mechanisms.
- Understanding these mechanisms provides a foundation for developing NDRG1-based cancer therapies.
- NDRG1's multifaceted inhibition of cancer cell migration and invasion underscores its therapeutic potential.
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