ArticleInternational journal of molecular sciences2020
Reactive Oxygen Species-Mediated Autophagy by Ursolic Acid Inhibits Growth and Metastasis of Esophageal Cancer Cells.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Ursolic acid in cancer therapy: a review of signaling pathways and apoptotic mechanisms.Molecular biology reports · 2026Review
- Ursolic acid as a multifunctional anticancer agent with insights into molecular mechanisms therapeutic potential and formulation strategies.Discover oncology · 2026Review
- Screening the Active Phytochemicals FromCancer innovation · 2025Review
- Modulation of Autophagy by Ursolic and Betulinic Acids: Distinct Cytotoxic and Membrane-Disruption in Malignant and Nonmalignant Cells.Cell biology international · 2025Article
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- Natural products for enhancing the sensitivity or decreasing the adverse effects of anticancer drugs through regulating the redox balance.Chinese medicine · 2024Review
- Role of ursolic acid in preventing gastrointestinal cancer: recent trends and future perspectives.Frontiers in pharmacology · 2024Review
- Ursolic Acid's Alluring Journey: One Triterpenoid vs. Cancer Hallmarks.Molecules (Basel, Switzerland) · 2023Review
- Inhibition of the interaction between Hippo/YAP and Akt signaling with ursolic acid and 3'3-diindolylmethane suppresses esophageal cancer tumorigenesis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Combination of Oncolytic Measles Virus and Ursolic Acid Synergistically Induces Oncolysis of Hepatocellular Carcinoma Cells.Viruses · 2023Article
- Rocuronium bromide suppresses esophageal cancer via blocking the secretion of C-X-C motif chemokine ligand 12 from cancer associated fibroblasts.Journal of translational medicine · 2023Article
- Unraveling the Complexity of Regulated Cell Death in Esophageal Cancer: from Underlying Mechanisms to Targeted Therapeutics.International journal of biological sciences · 2023Review
- Inhibition of colorectal cancer tumorigenesis by ursolic acid and doxorubicin is mediated by targeting the Akt signaling pathway and activating the Hippo signaling pathway.Molecular medicine reports · 2023Article
- Ursolic acid: a natural modulator of signaling networks in different cancers.Cancer cell international · 2022Review
- Recent Advances Regarding the Molecular Mechanisms of Triterpenic Acids: A Review (Part I).International journal of molecular sciences · 2022Review
- Ursolic Acid Accelerates Paclitaxel-Induced Cell Death in Esophageal Cancer Cells by Suppressing Akt/FOXM1 Signaling Cascade.International journal of molecular sciences · 2021Article
- Targeting Autophagy with Natural Compounds in Cancer: A Renewed Perspective from Molecular Mechanisms to Targeted Therapy.Frontiers in pharmacology · 2021Review
- Traditional Chinese Medicine Therapy for Esophageal Cancer: A Literature Review.Integrative cancer therapiesReview
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Ursolic acid (UA) possesses various pharmacological activities, such as antitumorigenic and anti-inflammatory effects. In the present study, we investigated the mechanisms underlying the effects of UA against esophageal squamous cell carcinoma (ESCC) (TE-8 cells and TE-12 cells). The cell viability assay showed that UA decreased the viability of ESCC in a dose-dependent manner. In the soft agar colony formation assay, the colony numbers and size were reduced in a dose-dependent manner after UA treatment. UA caused the accumulation of vacuoles and LC3 puncta, a marker of autophagosome, in a dose-dependent manner. Autophagy induction was confirmed by measuring the expression levels of LC3 and p62 protein in ESCC cells. UA increased LC3-II protein levels and decreased p62 levels in ESCC cells. When autophagy was hampered using 3-methyladenine (3-MA), the effect of UA on cell viability was reversed. UA also significantly inhibited protein kinase B (Akt) activation and increased p-Akt expression in a dose-dependent manner in ESCC cells. Accumulated LC3 puncta by UA was reversed after wortmannin treatment. LC3-II protein levels were also decreased after treatment with Akt inhibitor and wortmannin. Moreover, UA treatment increased cellular reactive oxygen species (ROS) levels in ESCC in a time- and dose-dependent manner. Diphenyleneiodonium (an ROS production inhibitor) blocked the ROS and UA induced accumulation of LC3-II levels in ESCC cells, suggesting that UA-induced cell death and autophagy are mediated by ROS. Therefore, our data indicate that UA inhibits the growth of ESCC cells by inducing ROS-dependent autophagy.
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