ArticleAnti-cancer drugs2014
Artemisinin triggers a G1 cell cycle arrest of human Ishikawa endometrial cancer cells and inhibits cyclin-dependent kinase-4 promoter activity and expression by disrupting nuclear factor-κB transcriptional signaling.
Article in Anti-cancer drugs, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 63 citations in OpenAlex.
- Natural bioactive compounds and herbal medicines targeting common signaling pathways in endometriosis: mechanisms and therapeutic implications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Exploring the Chemopreventive Potential ofPharmaceuticals (Basel, Switzerland) · 2024Article
- Curcumin potentiates the anti-inflammatory effects of Tehranolide by modulating the STAT3/NF-κB signaling pathway in breast and ovarian cancer cell lines.Inflammopharmacology · 2023Article
- Artesunate and cisplatin synergistically inhibit HNSCC cell growth and promote apoptosis with artesunate‑induced decreases in Rb and phosphorylated Rb levels.Oncology reports · 2023Article
- P53 Gene Expression and Nitric Oxide Levels after Artemisinin-Caffeine Treatment in Breast, Lungs and Liver of DMBA-Induced Tumorigenesis.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Artesunate, as an Hsp90 inhibitor, inhibits the proliferation of Burkitt's lymphoma cells by inhibiting AKT and ERK.Frontiers in pharmacology · 2023Article
- Sesquiterpenes fromMolecules (Basel, Switzerland) · 2022Article
- Endometrial Cancer Stem Cells: Where Do We Stand and Where Should We Go?International journal of molecular sciences · 2022Review
- Molecular insights into AabZIP1-mediated regulation on artemisinin biosynthesis and drought tolerance inActa pharmaceutica Sinica. B · 2022Article
- Artemisinin protects against cerebral ischemia and reperfusion injury via inhibiting the NF-κB pathway.Open medicine (Warsaw, Poland) · 2022Article
- Artemisinins in Combating Viral Infections Like SARS-CoV-2, Inflammation and Cancers and Options to Meet Increased Global Demand.Frontiers in plant science · 2022Review
- Artesunate Inhibits the Growth Behavior of Docetaxel-Resistant Prostate Cancer Cells.Frontiers in oncology · 2022Article
- Natural Kinase Inhibitors for the Treatment and Management of Endometrial/Uterine Cancer: Preclinical to Clinical Studies.Frontiers in pharmacology · 2022Review
- Worldwide Research Trends on Artemisinin: A Bibliometric Analysis From 2000 to 2021.Frontiers in medicine · 2022Article
- Upregulation of MicroRNA-34a Sensitizes Ovarian Cancer Cells to Resveratrol by Targeting Bcl-2.Yonsei medical journal · 2021Article
- Repurposing Artemisinin and its Derivatives as Anticancer Drugs: A Chance or Challenge?Frontiers in pharmacology · 2021Review
- Article
- Resveratrol Inhibits Proliferation in HBL-52 Meningioma Cells.OncoTargets and therapy · 2019Article
- Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine.Chinese medicine · 2019Review
- Resveratrol induces apoptosis in SGC-7901 gastric cancer cells.Oncology letters · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Relatively little is known about the antiproliferative effects of artemisinin, a naturally occurring antimalarial compound from Artemisia annua, or sweet wormwood, in human endometrial cancer cells. Artemisinin induced a G1 cell cycle arrest in cultured human Ishikawa endometrial cancer cells and downregulated cyclin-dependent kinase-2 (CDK2) and CDK4 transcript and protein levels. Analysis of CDK4 promoter-luciferase reporter constructs showed that the artemisinin ablation of CDK4 gene expression was accounted for by the loss of CDK4 promoter activity. Chromatin immunoprecipitation demonstrated that artemisinin inhibited nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) subunit p65 and p50 interactions with the endogenous Ishikawa cell CDK4 promoter. Coimmunoprecipitation revealed that artemisinin disrupts endogenous p65 and p50 nuclear translocation through increased protein-protein interactions with IκB-α, an NF-κB inhibitor, and disrupts its interaction with the CDK4 promoter, leading to a loss of CDK4 gene expression. Artemisinin treatment stimulated the cellular levels of IκB-α protein without altering the level of IκB-α transcripts. Finally, expression of exogenous p65 resulted in the accumulation of this NF-κB subunit in the nucleus of artemisinin-treated and artemisinin-untreated cells, reversed the artemisinin downregulation of CDK4 protein expression and promoter activity, and prevented the artemisinin-induced G1 cell cycle arrest. Taken together, our results demonstrate that a key event in the artemisinin antiproliferative effects in endometrial cancer cells is the transcriptional downregulation of CDK4 expression by disruption of NF-κB interactions with the CDK4 promoter.
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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.