ArticleBMC complementary and alternative medicine2014
Chebulagic acid from Terminalia chebula causes G1 arrest, inhibits NFκB and induces apoptosis in retinoblastoma cells.
Article in BMC complementary and alternative medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Molecular insights of a Unani formulation in targeting fibrosis-associated diseases.Frontiers in pharmacology · 2026Review
- Probable role of naturally derived bergapten molecule promotes autophagy in Mycobacterium tuberculosis-infected macrophages via PI3K/Akt/mTOR pathway.Archives of microbiology · 2025Article
- Potential Distribution Prediction ofEcology and evolution · 2025Article
- Chebulagic acid suppresses gastric cancer by inhibiting the AURKA/β-catenin/Wnt pathway.Frontiers in pharmacology · 2023Article
- Review
- Advances in the research of plant-derived natural products against retinoblastoma.International journal of ophthalmology · 2022Review
- Current advances on the phytochemical composition, pharmacologic effects, toxicology, and product development ofFrontiers in pharmacology · 2022Review
- Assessment of the Cytotoxic Activity of Triphala: A Semisolid Traditional Formulation on HepGBioMed research international · 2021Article
- MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1.Bioscience reports · 2020Article
- Virtual Screening Identifies Chebulagic Acid as an Inhibitor of the M2(S31N) Viral Ion Channel and Influenza A Virus.Molecules (Basel, Switzerland) · 2020Article
- Plants of the GenusFrontiers in pharmacology · 2020Review
- NF-κB p65 promotes ovarian cancer cell proliferation and migration via regulating mortalin.Journal of cellular and molecular medicine · 2019Article
- A Comprehensive Review of the Structure Elucidation of Tannins fromEvidence-based complementary and alternative medicine : eCAM · 2019Review
- Therapeutic targeting of oncogenic transcription factors by natural products in eye cancer.Pharmacological research · 2018Review
- Natural Compounds as Modulators of Cell Cycle Arrest: Application for Anticancer Chemotherapies.Current genomics · 2017Review
- Anticancer Natural Compounds as Epigenetic Modulators of Gene Expression.Current genomics · 2017Review
- Molecular mechanisms of cholangiocarcinoma cell inhibition by medicinal plants.Oncology letters · 2017Article
- Terminalia Chebula provides protection against dual modes of necroptotic and apoptotic cell death upon death receptor ligation.Scientific reports · 2016Article
- Natural compounds for pediatric cancer treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2016Review
- A Review on Potential Mechanisms of Terminalia chebula in Alzheimer's Disease.Advances in pharmacological sciences · 2016Review
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
backgroundPlants are the valuable source of natural products with important medicinal properties. Most of the approved anti cancer drugs have a natural product origin or are natural products. Retinoblastoma is the most common ocular cancer of children. Although chemotherapy is the preferred mode of therapy, a successful treatment for retinoblastoma requires enucleation. Chebulagic acid (CA) from Terminalia chebula was shown to have anti-proliferative properties in the studies on cancerous cell lines. Due to anti cancer properties of CA and due to limitation in treatment options for retinoblastoma, the present study is undertaken to understand the role of CA on the proliferation of retinoblastoma cells.
methodsAnti proliferative potential of CA was determined by MTT assay. The expression levels of various cell death mediators in retinoblastoma cells with CA treatment were assessed by Western blotting. Flowcytometer analysis was used to estimate the mitochondrial membrane potential (MMP) and to determine the percentage of cells undergoing apoptosis.
resultsThe present study showed CA inhibited the proliferation of retinoblastoma cells in a dose dependent manner. CA modulated MMP, induced release of Cytochrome c, activated caspase 3 and shifted the ratio of BAX and Bcl2 towards cell death. G1 arrest, noticed in CA treated cells, is mediated by the increase in the expression of CDK inhibitor p27. CA treatment also decreased the levels of NFκB in the nucleus. This decrease is mediated by suppression in degradation of IκBα.
conclusionCA has shown significant anti proliferative potential on retinoblastoma cells. Our findings clearly demonstrate that CA induces G1 arrest, inhibits NFκB and induces apoptosis of retinoblastoma cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.