ArticleExperimental and therapeutic medicine2018
Gambogic acid regulates the migration and invasion of colorectal cancer via microRNA-21-mediated activation of phosphatase and tensin homolog.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Plant-Derived Secondary Metabolites Modulating Inflammation-Driven Pathways in Hepatocellular Carcinoma: Preclinical Insights.Current issues in molecular biology · 2026Review
- Crosstalk between non-coding RNAs and programmed cell death in colorectal cancer: implications for targeted therapy.Epigenetics & chromatin · 2025Review
- Review
- Emerging tendencies for the nano-delivery of gambogic acid: a promising approach in oncotherapy.RSC advances · 2024Review
- Xanthones fromInternational journal of molecular sciences · 2023Article
- Article
- Participation of MicroRNAs in the Treatment of Cancer with Phytochemicals.Molecules (Basel, Switzerland) · 2020Review
- Gambogic acid: A shining natural compound to nanomedicine for cancer therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2020Review
- Gambogic Acid as a Candidate for Cancer Therapy: A Review.International journal of nanomedicine · 2020Review
- Levosimendan Protects against Doxorubicin-Induced Cardiotoxicity by Regulating the PTEN/Akt Pathway.BioMed research international · 2020Article
- Gambogic acid suppresses colon cancer cell activityExperimental and therapeutic medicine · 2019Article
- Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine.Chinese medicine · 2019Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gambogic acid (GA) has been reported to inhibit cancer cell proliferation and migration and enhance apoptosis. Several signaling pathways were identified to be involved in GA function, including PI3K/Akt, caspase-3 apoptosis and TNF-α/NF-κB. However, to the best of our knowledge, the association between miRNA and GA has not been explored. The present study initially demonstrated that GA could inhibit HT-29 cancer cell proliferation using an MTT assay. In addition, a Transwell assay and a wound-healing assay respectively indicated that GA inhibited HT-29 cancer cell invasion and migration, which was also confirmed by the increased MMP-9 protein expression. Furthermore, GA induced the apoptosis of HT-29 cancer cells in an Annexin V and PI double staining assay. Moreover, treatment with GA significantly decreased miR-21 expression in these cells. Additionally, western blot analysis demonstrated that GA treatment enhanced the activation of phosphatase and tensin homolog (PTEN) along with the suppression of PI3K and p-Akt. Furthermore, miR-21 mimics reversed all the aforementioned activities of GA, which indicated that miR-21 was the effector of GA and blocked PI3K/Akt signaling pathway via enhancing PTEN activity. In summary, GA induced HT-29 cancer cell apoptosis via decreasing miR-21 expression and blocking PI3K/Akt, which may be a useful novel insight for future CRC treatment.
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