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Feiwei Mixture Exerts Antitumor Activity Against Non-Small Cell Lung Cancer via Regulating NR1D1-Mediated Immune Cell
Haiyong Wang1, Lingsun Guo2, Yu Zhao3
1Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China.
Advanced Biology
|February 23, 2026
Summary
Feiwei Mixture (FWHJ) inhibits non-small cell lung cancer (NSCLC) by activating NR1D1, boosting anti-tumor immunity via the cGAS-STING pathway and suppressing JAK-STAT3 signaling. This reveals FWHJ
Area of Science:
- Immunology
- Oncology
- Pharmacology
Background:
- Feiwei Mixture (FWHJ) is a hospital preparation for lung cancer with an undefined mechanism of action.
- Understanding FWHJ's molecular targets is crucial for optimizing lung cancer therapy.
Purpose of the Study:
- To elucidate the anti-tumor mechanism of FWHJ in non-small cell lung cancer (NSCLC).
- To investigate the role of NR1D1, cGAS-STING, and JAK-STAT3 signaling in FWHJ's therapeutic effects.
Main Methods:
- Lewis lung carcinoma (LLC) tumor-bearing mice and LLC-CD8+ T cell co-culture models were utilized.
- Western blot, flow cytometry, and immunoassays assessed tumor growth, T cell infiltration, apoptosis, and key signaling molecules.
- NR1D1 knockout models were employed to confirm its role.
Main Results:
- FWHJ dose-dependently inhibited tumor growth and enhanced CD4+/CD8+ T cell infiltration in vivo.
- FWHJ upregulated NR1D1, SOCS3, and the cGAS-STING pathway, while suppressing JAK-STAT3 signaling.
- NR1D1 knockout abrogated FWHJ's anti-tumor effects, confirming its essential role.
Conclusions:
- FWHJ exerts anti-NSCLC effects by activating NR1D1, stimulating the cGAS-STING pathway, and suppressing JAK-STAT3 signaling.
- This mechanism enhances anti-tumor immunity, providing a scientific basis for FWHJ in lung cancer treatment.
