ArticleFrontiers in oncology2021
Multitargeting Effects of Calebin A on Malignancy of CRC Cells in Multicellular Tumor Microenvironment.
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Multifunctionality of Calebin A in inflammation, chronic diseases and cancer.Frontiers in oncology · 2022Pooled it
- An Overview of the Pharmacological Properties of Calebin-A.Current medicinal chemistry · 2025Review
- Effect of Calebin-A on Critical Genes Related to NAFLD: A Protein-Protein Interaction Network and Molecular Docking Study.Current genomics · 2024Article
- Delineating the role of nuclear receptors in colorectal cancer, a focused review.Discover oncology · 2024Review
- Exploring the nexus of nuclear receptors in hematological malignancies.Cellular and molecular life sciences : CMLS · 2024Review
- Calebin A modulates inflammatory and autophagy signals for the prevention and treatment of osteoarthritis.Frontiers in immunology · 2024Article
- B7H3 Role in Reshaping Immunosuppressive Landscape in MSI and MSS Colorectal Cancer Tumours.Cancers · 2023Article
- Augmentation of Docetaxel-Induced Cytotoxicity in Human PC-3 Androgen-Independent Prostate Cancer Cells by Combination With Four Natural Apoptosis-Inducing Anticancer Compounds.Natural product communications · 2023Article
- Resveratrol Modulates Chemosensitisation to 5-FU via β1-Integrin/HIF-1α Axis in CRC Tumor Microenvironment.International journal of molecular sciences · 2023Article
- Resveratrol induces apoptosis by modulating the reciprocal crosstalk between p53 and Sirt-1 in the CRC tumor microenvironment.Frontiers in immunology · 2023Article
- Calebin A targets the HIF-1α/NF-κB pathway to suppress colorectal cancer cell migration.Frontiers in pharmacology · 2023Article
- Oroxylin A: A Promising Flavonoid for Prevention and Treatment of Chronic Diseases.Biomolecules · 2022Review
- Evidence That β1-Integrin Is Required for the Anti-Viability and Anti-Proliferative Effect of Resveratrol in CRC Cells.International journal of molecular sciences · 2022Article
- Bacteria-Mediated Modulatory Strategies for Colorectal Cancer Treatment.Biomedicines · 2022Review
- Exosome application in tumorigenesis: diagnosis and treatment of melanoma.Medical oncology (Northwood, London, England) · 2022Review
- Anti-Inflammatory and Anticancer Properties of Birch Bark-Derived Betulin: Recent Developments.Plants (Basel, Switzerland) · 2021Review
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
backgroundTumor microenvironment (TME) provides the essential prerequisite niche for promoting cancer progression and metastasis. Calebin A, a component of
methods3D-alginate tumor cultures (HCT116 cells) in the multicellular proinflammatory TME (fibroblast cells/T lymphocytes), tumor necrosis factor beta (TNF-β)-TME (fibroblast cells/TNF-β) were treated with/without Calebin A to address the pleiotropic actions of Calebin A in the CRC.
resultsWe found that Calebin A downmodulated proliferation, vitality, and migration of HCT116 cells in 3D-alginate cultures in multicellular proinflammatory TME or TNF-β-TME. In addition, Calebin A suppressed TNF-β-, similar to multicellular-TME-induced phosphorylation of nuclear factor kappa B (NF-κB) in a concentration-dependent manner. NF-κB-promoting proinflammatory mediators, associated with tumor growth and antiapoptotic molecules (i.e.,MMP-9, CXCR4, Ki-67, β1-integrin, and Caspase-3) and its translocation to the nucleus in HCT116 cells, were increased in both TME cultures. The multicellular-TME cultures further induced the survival of cancer stem cells (CSCs) (upregulation of CD133, CD44, and ALDH1). Last but not the least, Calebin A suppressed multicellular-, similar to TNF-β-TME-induced rigorous upregulation of NF-κB phosphorylation, various NF-κB-regulated gene products, CSCs activation, and survival in 3D-alginate tumor cultures.
conclusionsThe downmodulation of multicellular proinflammatory-, similar to TNF-β-TME-induced CRC proliferation, survival, and migration by the multitargeting agent Calebin A could be a new therapeutic strategy to suppress inflammation and CRC tumorigenesis.
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