ArticleOncology letters2016
Anticancer effect of icaritin inhibits cell growth of colon cancer through reactive oxygen species, Bcl-2 and cyclin D1/E signaling.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Icaritin suppresses CAD-mediated liver cancer development by targeting miR-18b-5p in a xenograft mouse model.Medical oncology (Northwood, London, England) · 2025Article
- Mitochondrial DNA copy number alterations: Key players in the complexity of glioblastoma (Review).Molecular medicine reports · 2025Review
- Icariin Inhibits Lung Adenocarcinoma Progression Through TP53-Mediated Ferroptosis.OncoTargets and therapy · 2025Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Transplant oncology and anti-cancer immunosuppressants.Frontiers in immunology · 2024Review
- Icaritin inhibits PLK1 to activate DNA damage response in NK/T cell lymphoma and increases sensitivity to GELOX regime.Molecular therapy oncolytics · 2022Article
- Exploring the pharmacological mechanisms of icaritin against nasopharyngeal carcinomaFrontiers in pharmacology · 2022Article
- A comparative study on theDrug delivery · 2020Article
- Natural and herbal compounds targeting breast cancer, a review based on cancer stem cells.Iranian journal of basic medical sciences · 2020Review
- Kaposi Sarcoma-Associated Herpesvirus and Staphylococcus aureus Coinfection in Oral Cavities of HIV-Positive Patients: A Unique Niche for Oncogenic Virus Lytic Reactivation.The Journal of infectious diseases · 2020Article
- Knockdown of lncRNA MCM3AP-AS1 Attenuates Chemoresistance of Burkitt Lymphoma to Doxorubicin Treatment via Targeting the miR-15a/EIF4E Axis.Cancer management and research · 2020Article
- Induction of ROS and DNA damage-dependent senescence by icaritin contributes to its antitumor activity in hepatocellular carcinoma cells.Pharmaceutical biology · 2019Article
- MicroRNA‑25/ATXN3 interaction regulates human colon cancer cell growth and migration.Molecular medicine reports · 2019Article
- Reactive oxygen species induced by icaritin promote DNA strand breaks and apoptosis in human cervical cancer cells.Oncology reports · 2019Article
- In a Rat Model of Acute Liver Failure, Icaritin Improved the Therapeutic Effect of Mesenchymal Stem Cells by Activation of the Hepatocyte Growth Factor/c-Met Pathway.Evidence-based complementary and alternative medicine : eCAM · 2019Article
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Icaritin has an advantage in enhancing immunity. Besides, with its anticancer effect, it may be of great help in cancer treatment and recovery of cancer patients. As a result, icaritin is likely to become a novel anticancer drug. However, the anticancer effect of icaritin against colon cancer has not been elucidated thus far. The present study investigated the latent anticancer effect of icaritin on the inhibition of colon cancer cell growth by regulating reactive oxygen species (ROS), B-cell lymphoma (Bcl)-2 and cyclin D1/E signaling. The COLO-205 colon cancer cell line was used as a colon cancer cell model in the present study. First, cell growth and apoptosis were measured to analyze the anticancer effect of icaritin against colon cancer. Next, the possible mechanism of icaritin against colon cancer, including ROS, Bcl-2, cyclin D1, cyclin E and caspase-3/9, was explored. The results revealed that icaritin could inhibit cell growth and induce the apoptosis of COLO-205 cells. In addition, icaritin significantly induced ROS generation, suppressed Bcl-2, cyclin D1 and cyclin E protein expression, and activated caspase-3/9 activity in COLO-205 cells. The present findings demonstrated that icaritin exerted antiproliferative and anticancer effects against colon cancer through the activation of ROS generation and the suppression of Bcl-2, cyclin D1 and cyclin E signaling.
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