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Review
. 2025 Oct;54(4):126.
doi: 10.3892/or.2025.8959. Epub 2025 Aug 1.

Advances in the chemo‑preventive effects and mechanisms of ursolic acid against lung cancer (Review)

Zhanyu Lin  1 , Qingze Chen  1 , Zhaoyue Chen  2 , Tianyang Peng  2 , Jinglu Bai  1 , Fengjun Ma  2
Affiliations
Review

Advances in the chemo‑preventive effects and mechanisms of ursolic acid against lung cancer (Review)

Zhanyu Lin et al. Oncol Rep. 2025 Oct.

Abstract

Ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, exhibits diverse biological activities and notable antitumor properties. Lung cancer (LC), a leading malignancy of the respiratory system, is predominantly classified into small cell LC and non‑small cell LC. The increasing incidence and mortality rates of LC have spurred considerable interest in the chemo‑preventive potential of UA. Accumulating evidence demonstrates that UA markedly inhibits LC cell proliferation and induces apoptosis. Mechanistically, UA induces cell cycle arrest at the G0/G1 phase, thereby suppressing LC cell invasion, migration and tumor growth. Furthermore, UA has shown synergistic effects when combined with other therapeutic agents, including mitotic kinase inhibitors and multifunctional nanomedicines, effectively overcoming drug resistance in LC cells. These multifaceted mechanisms collectively contribute to the chemo‑preventive efficacy of UA against LC. Consequently, UA represents a promising candidate for LC prevention and therapy. The present review comprehensively summarizes the anticancer effects and molecular mechanisms of UA in LC, offering insights to guide future research and facilitate the development of innovative therapeutic strategies.

Keywords: chemoprevention; lung cancer; phytomedicine; respiratory diseases; ursolic acid.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1. Molecular targets regulated by UA and their effects on cellular autophagy and apoptosis. UA, ursolic acid; HA–Lipo / UA, hyaluronic acid–liposome UA; GSH, glutathione; MMP, matrix metallopro...
Figure 1.
Molecular targets regulated by UA and their effects on cellular autophagy and apoptosis. UA, ursolic acid; HA-Lipo/UA, hyaluronic acid-liposome UA; GSH, glutathione; MMP, matrix metalloproteinase; ARTS, apoptosis-related protein in the TGF-β signaling pathway; HIF, hypoxia-inducible factor; PD-L1, programmed death-ligand 1; VRK1, vaccinia-related kinase 1; Chop, C/EBP-homologous protein. Figure created using Adobe Illustrator 2024 (v28.0), Adobe Inc.
Figure 2. Molecular targets regulated by UA and their effects on cell invasion and migration. UA, ursolic acid; MMP, matrix metalloproteinase; AEG–1, astrocyte–elevated gene–1. Figure created using Ad...
Figure 2.
Molecular targets regulated by UA and their effects on cell invasion and migration. UA, ursolic acid; MMP, matrix metalloproteinase; AEG-1, astrocyte-elevated gene-1. Figure created using Adobe Illustrator 2024 (v28.0), Adobe Inc.
Figure 3. Molecular targets regulated by UA and their effects on cell proliferation. UA, ursolic acid. Figure created using Adobe Illustrator 2024 (v28.0), Adobe Inc.
Figure 3.
Molecular targets regulated by UA and their effects on cell proliferation. UA, ursolic acid. Figure created using Adobe Illustrator 2024 (v28.0), Adobe Inc.
Figure 4. Molecular targets regulated by UA and their impact on attenuating drug resistance. UA, ursolic acid; miR, microRNA. Figure created using Adobe Illustrator 2024 (v28.0), Adobe Inc.
Figure 4.
Molecular targets regulated by UA and their impact on attenuating drug resistance. UA, ursolic acid; miR, microRNA. Figure created using Adobe Illustrator 2024 (v28.0), Adobe Inc.
Figure 5. Mechanisms associated with the chemoprotective effect of UA for the treatment of lung cancer. UA, ursolic acid. Figure created using Adobe Illustrator 2024 (v28.0), Adobe Inc.
Figure 5.
Mechanisms associated with the chemoprotective effect of UA for the treatment of lung cancer. UA, ursolic acid. Figure created using Adobe Illustrator 2024 (v28.0), Adobe Inc.
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