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Updated: Dec 17, 2025

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
The oncogenic role of Jagged1/Notch signaling in cancer
Meng-Xi Xiu1, Yuan-Meng Liu1, Bo-Hai Kuang1
1Medical School of Nanchang University, 603 Bayi Road, Nanchang, Jiangxi 330006, China.
Abstract:
Aberrant activation of Notch signaling plays an oncogenic role in cancer development. Jagged1 (JAG1) is an important Notch ligand that triggers Notch signaling through cell-cell interactions. JAG1 overexpression has been reported in many different types of cancer and correlates with a poor clinical prognosis. JAG1/Notch signaling controls oncogenic processes in different cell types and cellular contexts. Furthermore, JAG1/Notch signaling cascades activate a number of oncogenic factors that regulate cellular functions such as proliferation, metastasis, drug-resistance, and angiogenesis. To suppress the severe toxicity of pan-Notch inhibitors, JAG1 is attracting increasing attention as a source of therapeutic targets for cancers. In this review, the oncogenic role of JAG1/Notch signaling in cancer is discussed, as well as implications of strategies to inhibit JAG1/Notch signaling activity.
Insights
Aberrant Notch signaling, driven by Jagged1 (JAG1), promotes cancer. Inhibiting JAG1 offers a promising therapeutic strategy for various cancers, potentially reducing toxicity associated with broader Notch pathway inhibitors.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Signaling Pathways
Background:
- Aberrant activation of Notch signaling is a key driver in cancer development.
- Jagged1 (JAG1), a Notch ligand, is frequently overexpressed in cancers and linked to poor prognosis.
- JAG1/Notch signaling regulates critical oncogenic processes including proliferation, metastasis, drug resistance, and angiogenesis.
Purpose of the Study:
- To review the oncogenic role of Jagged1 (JAG1)/Notch signaling in cancer.
- To discuss the implications of JAG1 as a therapeutic target for cancer treatment.
- To explore strategies for inhibiting JAG1/Notch signaling activity to overcome pan-Notch inhibitor toxicity.
Main Methods:
- Literature review synthesizing current research on JAG1/Notch signaling in cancer.
- Analysis of the oncogenic functions regulated by JAG1/Notch cascades.
- Evaluation of therapeutic strategies targeting JAG1.
Main Results:
- JAG1 overexpression is a significant factor in multiple cancer types, correlating with adverse clinical outcomes.
- JAG1/Notch signaling pathways activate oncogenic factors essential for tumor progression and resistance.
- Targeting JAG1 presents a more specific approach compared to pan-Notch inhibitors, potentially mitigating severe toxicities.
Conclusions:
- JAG1/Notch signaling is a critical oncogenic pathway in cancer development and progression.
- JAG1 represents a valuable therapeutic target for developing novel anti-cancer strategies.
- Inhibiting JAG1 offers a promising avenue for cancer therapy with potentially reduced side effects.
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