ArticleBiomedicines2020
Targeting NF-κB Signaling by Calebin A, a Compound of Turmeric, in Multicellular Tumor Microenvironment: Potential Role of Apoptosis Induction in CRC Cells.
Article in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Multifunctionality of Calebin A in inflammation, chronic diseases and cancer.Frontiers in oncology · 2022Pooled it
- Calebin A mitigates oxidative stress and inflammation in diabetic nephropathy via Nrf2/HO-1 and NF-κB signaling pathways.Journal of diabetes investigation · 2026Article
- Harnessing nanomedicine to target NF-κB signalling in cancer: at the intersection of inflammatory signalling, metabolic reprogramming, and therapeutic innovation.Cell communication and signaling : CCS · 2026Review
- Advancements in Enteric-coated Microspheres Formulation Development and Mangiferin Drug Delivery for the Treatment of Ulcerative Colitis.Recent advances in drug delivery and formulation · 2026Article
- The dual facets of MiRNA in modulating NF-κB in breast cancer.Cancer cell international · 2025Review
- Synergistic effects of Calebin A and docetaxel on apoptosis and migration in prostate cancer cells.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2025Article
- Comprehensive review of leonurine: harnessing its therapeutic potential for chronic diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Adipo-Modulation by Turmeric Bioactive Phenolic Components: From Curcuma Plant to Effects.International journal of molecular sciences · 2025Review
- Deciphering the metabolic landscape of colorectal cancer through the lens of AhR-mediated intestinal inflammation.Discover oncology · 2025Review
- An Overview of the Pharmacological Properties of Calebin-A.Current medicinal chemistry · 2025Review
- Regulating the regulators: long non-coding RNAs as autophagic controllers in chronic disease management.Journal of biomedical science · 2024Review
- Cell plasticity modulation by flavonoids in resistant breast carcinoma targeting the nuclear factor kappa B signaling.Cancer metastasis reviews · 2024Review
- Metabolic and Genetic Association of Vitamin D with Calcium Signaling and Insulin Resistance.Indian journal of clinical biochemistry : IJCB · 2023Review
- Calebin-A prevents HFD-induced obesity in mice by promoting thermogenesis and modulating gut microbiota.Journal of traditional and complementary medicine · 2023Article
- Calebin A targets the HIF-1α/NF-κB pathway to suppress colorectal cancer cell migration.Frontiers in pharmacology · 2023Article
- Unraveling the Potential Role of NEDD4-like E3 Ligases in Cancer.International journal of molecular sciences · 2022Review
- The Novel Protein ADAMTS16 Promotes Gastric Carcinogenesis by Targeting IFI27 through the NF-κb Signaling Pathway.International journal of molecular sciences · 2022Article
- Demystifying the Functional Role of Nuclear Receptors in Esophageal Cancer.International journal of molecular sciences · 2022Review
- Oroxylin A: A Promising Flavonoid for Prevention and Treatment of Chronic Diseases.Biomolecules · 2022Review
- Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing lines of evidence suggest that chronic inflammation mediates most chronic diseases, including cancer. The transcription factor, NF-κB, has been shown to be a major regulator of inflammation and metastasis in tumor cells. Therefore, compounds or any natural agents that can inhibit NF-κB activation have the potential to prevent and treat cancer. However, the mechanism by which Calebin A, a component of turmeric, regulates inflammation and disrupts the interaction between HCT116 colorectal cancer (CRC) cells and multicellular tumor microenvironment (TME) is still poorly understood. The 3D-alginate HCT116 cell cultures in TME were treated with Calebin A, BMS-345541, and dithiothreitol (DTT) and examined for invasiveness, proliferation, and apoptosis. The mechanism of TME-induced malignancy of cancer cells was confirmed by phase contrast, Western blotting, immunofluorescence, and DNA-binding assay. We found through DNA binding assay, that Calebin A inhibited TME-induced NF-κB activation in a dose-dependent manner. As a result of this inhibition, NF-κB phosphorylation and NF-κB nuclear translocation were down-modulated. Calebin A, or IκB-kinase (IKK) inhibitor (BMS-345541) significantly inhibited the direct interaction of nuclear p65 to DNA, and interestingly this interaction was reversed by DTT. Calebin A also suppressed the expression of NF-κB-promoted anti-apoptotic (Bcl-2, Bcl-xL, survivin), proliferation (Cyclin D1), invasion (MMP-9), metastasis (CXCR4), and down-regulated apoptosis (Caspase-3) gene biomarkers, leading to apoptosis in HCT116 cells. These results suggest that Calebin A can suppress multicellular TME-promoted CRC cell invasion and malignancy by inhibiting the NF-κB-promoting inflammatory pathway associated with carcinogenesis, underlining the potential of Calebin A for CRC treatment.
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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.