ArticleCancer letters2015
Baicalein upregulates DDIT4 expression which mediates mTOR inhibition and growth inhibition in cancer cells.
Article in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed.
- Enhancer-mediated DDIT4 activation by SMYD2-dependent H3K4me1 promotes pazopanib resistance in clear cell renal cell carcinoma.Journal of translational medicine · 2026Article
- Pharmacological targets and mechanism of baicalein in treating breast cancer: a study based on network pharmacology, molecular docking, and bioinformatics analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Elucidating the Molecular Network Underpinning Hypoxia Adaptation in the Liver of Silver Carp (Animals : an open access journal from MDPI · 2025Article
- Therapeutic Potential of Baicalein in Endometrial Cancer: Suppression of mTOR Signaling and Synergy with Metformin.International journal of molecular sciences · 2025Article
- Therapeutic effect of baicalein as an antiparasitic agent againstJournal of Zhejiang University. Science. B · 2025Article
- Lower cytoplasmic expression of DDIT4 is associated with poor prognosis in gastric cancer patients.Discover oncology · 2025Article
- The Therapeutic Potential of Baicalin and Baicalein in Breast Cancer: A Systematic Review of Mechanisms and Efficacy.Current issues in molecular biology · 2025Review
- Increased nuclear expression of DNA damage inducible transcript 4 can serve as a potential prognostic biomarker in patients with gliomas: a study based on data mining and experimental tools.Discover oncology · 2025Article
- Targeting MMR-deficient colorectal cancer with a potent small molecule UNI110.Animal cells and systems · 2025Article
- Integrated Single-Cell and Spatial Transcriptomic Analysis Identifies ISR-Related Genes Driving Immune Regulation in Parkinson's Disease.Journal of inflammation research · 2025Article
- The diagnostic and prognostic value ofBioImpacts : BI · 2025Article
- Phenformin activates ER stress to promote autophagic cell death via NIBAN1 and DDIT4 in oral squamous cell carcinoma independent of AMPK.International journal of oral science · 2024Article
- Romidepsin exhibits anti-esophageal squamous cell carcinoma activity through the DDIT4-mTORC1 pathway.Cancer gene therapy · 2024Article
- NET-related gene signature for predicting AML prognosis.Scientific reports · 2024Article
- Nuclear overexpression of DNA damage-inducible transcript 4 (DDIT4) is associated with aggressive tumor behavior in patients with pancreatic tumors.Scientific reports · 2023Article
- PENALIZED REGRESSION FOR MULTIPLE TYPES OF MANY FEATURES WITH MISSING DATA.Statistica Sinica · 2023Article
- Some Nanocarrier's Properties and Chemical Interaction Mechanisms with Flavones.Molecules (Basel, Switzerland) · 2023Review
- Blueberry Anthocyanins from Commercial Products: Structure Identification and Potential for Diabetic Retinopathy Amelioration.Molecules (Basel, Switzerland) · 2022Article
- Flavones: Six Selected Flavones and Their Related Signaling Pathways That Induce Apoptosis in Cancer.International journal of molecular sciences · 2022Review
- Regulation of Cell Signaling Pathways and Non-Coding RNAs by Baicalein in Different Cancers.International journal of molecular sciences · 2022Review
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Authors and funding
15 authors.
Funding
Abstract
Baicalein is a natural flavone that exhibits anticancer properties. Using microarrays we found that DDIT4 was the highest transcript induced by baicalein in cancer cells. We confirmed in multiple cancer cell lines large, dose-related expression of DDIT4 by quantitative RT-PCR and immunoblot, which correlates with growth inhibition. Time course experiments demonstrate that DDIT4 is rapidly inducible, with high expression maintained for several days in vitro. Induction of DDIT4 expression is p53 independent based on evaluation of p53 knockout cells. Since DDIT4 is known to inhibit mTORC1 activity we confirmed that baicalein suppresses phosphorylation of mTORC1 targets. Using RNA interference we demonstrate that mTORC1 activity and growth inhibition by baicalein is attenuated by knockdown of DDIT4. We furthermore demonstrate suppression of established tumors by baicalein in a mouse model of breast cancer with increased DDIT4 expression in the tumors. Finally, we demonstrate that baicalein upregulates DDIT4 and causes mTORC1 and growth inhibition in platinum resistant cancer cells in marked contrast to platinum chemotherapy treatment. These studies demonstrate that baicalein inhibits mTORC1 through DDIT4 expression, and may be useful in cancer chemotherapy and chemoprevention.
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