ArticleIranian journal of pharmaceutical research : IJPR
Hyaluronic Acid-modified Liposomes for Ursolic Acid-targeted Delivery Treat Lung Cancer Based on p53/ARTS-mediated Mitochondrial Apoptosis.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Antimicrobial Activity Versus Virulence Potential of Hyaluronic Acid: Balancing Advantages and Disadvantages.International journal of molecular sciences · 2025Review
- Advances in the chemo‑preventive effects and mechanisms of ursolic acid against lung cancer (Review).Oncology reports · 2025Review
- Therapeutic Potential of Wogonin-Aloperine Co-Amorphous for Oral Squamous Cell Carcinoma.Pharmaceutics · 2025Article
- Ursolic acid in colorectal cancer: mechanisms, current status, challenges, and future research directions.Pharmacological reports : PR · 2025Review
- BTF3 affects hepatocellular carcinoma progression by transcriptionally upregulating PDCD2L and inactivating p53 signaling.Molecular medicine (Cambridge, Mass.) · 2024Article
- Hyaluronic acid-modified liposomes PotentiatedFrontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chemotherapy drugs can cause drug resistance and other problems when treating lung cancer, which leads to treatment failure. Ursolic acid (UA) is used in formulations based on traditional Chinese medicine. UA has excellent anti-tumor effects, but they are limited by solubility and non-specificity to tumor cells. Objectives: To overcome these issues, we created a novel hyaluronic acid (HA)-targeted liposome system for delivering UA (HA-Lipo/UA) to explore the targeting and anti-tumor effects of UA. Methods: We constructed the HA-Lipo/UA delivery system by the thin film hydration method. The uptake and localization of UA were detected by flow cytometry and microscope. Cell proliferation of A549 cells was detected by MTT assays. Apoptosis and reactive oxygen species (ROS) expression of A549 cells were also evaluated after being treated with HA-Lipo/UA. Western blot analysis evaluated the anti-tumor mechanism of HA-Lipo/UA. Results: HA-Lipo/UA exhibited favorable targeting of the cluster of differentiation (CD)44-overexpressing A549 cells. HA-Lipo/UA exhibited significant inhibition of the proliferation of A549 cells and induced their apoptosis compared with the corresponding monotherapies. HA-Lipo/UA induced overexpression of reactive oxygen species and upregulated expression of p53 and apoptosis-related protein in the transforming growth factor-β signaling (ARTS) pathway, which induced cytochrome-c release, activation of caspase-3, and promoted mitochondrial apoptosis in A549 cells. Conclusions: Taken together, these data suggested that HA-Lipo/UA could be used to target tumor cells.
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