ArticleMolecular medicine reports2015
Ponicidin suppresses HT29 cell growth via the induction of G1 cell cycle arrest and apoptosis.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 26 citations in OpenAlex.
- Semisynthesis and Antitumour Evaluation of Natural Derivatives fromInternational journal of molecular sciences · 2024Article
- Ponicidin Promotes Hepatocellular Carcinoma Mitochondrial Apoptosis by Stabilizing Keap1-PGAM5 Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Chlorogenic acid induces apoptosis and cell-cycle arrest in colorectal cancer cells.Molecular biology reports · 2023Article
- Molecular Mechanistic Pathways Targeted by Natural Compounds in the Prevention and Treatment of Diabetic Kidney Disease.Molecules (Basel, Switzerland) · 2022Review
- Ponicidin Treatment Improved the Cell Proliferation, Differentiation, and Calcium Mineralization on the Osteoblast-Like MG-63 Cells.Applied biochemistry and biotechnology · 2022Article
- Mechanistic Pathways and Molecular Targets of Plant-Derived AnticancerBiomolecules · 2020Review
- Ponicidin inhibits pro-inflammatory cytokine TNF-α-induced epithelial-mesenchymal transition and metastasis of colorectal cancer cells via suppressing the AKT/GSK-3β/Snail pathway.Inflammopharmacology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ponicidin is a diterpenoid extracted from the Chinese herb Isodon adenolomus, which has been reported as a therapeutic cytotoxic drug that may be used to treat various types of human cancer. The present study aimed to determine the antitumor effects of ponicidin, and to investigate its underlying mechanisms in colorectal cancer. The HT29 colorectal cancer cell line was used to detect the cytotoxicity of various doses of ponicidin. Cell proliferation was measured using a Cell Counting kit‑8 assay. Cell cycle and apoptosis analyses were performed using flow cytometry and fluorescent microscopy. Western blot analysis was used to measure the expression levels of apoptosis‑associated proteins following treatment with ponicidin. Treatment with ponicidin significantly suppressed HT29 cell growth by inducing G1 cell cycle arrest and apoptosis. The AKT and MEK signaling pathways were also suppressed by ponicidin; however, the p38 signaling pathway was significantly activated. The expression levels of caspase 3 and Bax protein were markedly upregulated following treatment with ponicidin. These results suggest that ponicidin exerts significant antitumor effects via the induction of cell cycle arrest and apoptosis in colorectal cells. In conclusion, ponicidin acted as an inducer of apoptosis, and may be used as a therapeutic cytotoxic drug to treat human cancer, including colorectal cancer.
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