ArticleMediators of inflammation2016
GEN-27, a Newly Synthetic Isoflavonoid, Inhibits the Proliferation of Colon Cancer Cells in Inflammation Microenvironment by Suppressing NF-κB Pathway.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Polyphenol Intake in Elderly Patients: A Novel Approach to Counteract Colorectal Cancer Risk?International journal of molecular sciences · 2025Review
- Isoflavones: Promising Natural Agent for Cancer Prevention and Treatment.Food science & nutrition · 2025Review
- Antioxidant Role of Probiotics in Inflammation-Induced Colorectal Cancer.International journal of molecular sciences · 2024Review
- Modulation of the tumor microenvironment by natural agents: implications for cancer prevention and therapy.Seminars in cancer biology · 2022Review
- Cancer cell metabolic plasticity in migration and metastasis.Clinical & experimental metastasis · 2021Review
- The Hallmarks of Flavonoids in Cancer.Molecules (Basel, Switzerland) · 2021Review
- The Role of Interleukins in Colorectal Cancer.International journal of biological sciences · 2020Review
- RNA Expression Profile and Alternative Splicing Signatures of Genistein-Treated Breeder Hens Revealed by Hepatic Transcriptomic Analysis.Oxidative medicine and cellular longevity · 2019Article
- Recent progress on the effects of microRNAs and natural products on tumor epithelial-mesenchymal transition.OncoTargets and therapy · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonresolving inflammation is one of the consistent features of the tumor microenvironment in the intestine and plays a critical role in the initiation and development of colon cancer. Here we reported the inhibitory effects of GEN-27, a new derivative of genistein, on the inflammation-related colon cancer cell proliferation and delineated the mechanism of its action. The results indicated that GEN-27 inhibited the proliferation of human colon tumor HCT116 cells stimulated by culture supernatants of LPS-induced human monocytes THP-1 cells and significantly decreased LPS-induced secretion of proinflammatory cytokines interleukin-6 and interleukin-1β in THP-1 cells. The HCT116 cell proliferation elicited by THP-1-conditioned medium could be blocked by the interleukin-1 receptor antagonist (IL-1RA). Further mechanistic study revealed that GEN-27 remarkably inhibited the nuclear translocation of NF-κB and phosphorylation of IκB and IKKα/β in both HCT116 and THP-1 cells. In addition, GEN-27 markedly suppressed the HCT116 cell proliferation stimulated by IL-1β treatment, which was dependent on the inhibition of NF-κB/p65 nuclear localization, as verified by p65 overexpression and BAY 11-7082, an NF-κB inhibitor. Taken together, our findings established that GEN-27 modulated NF-κB signaling pathway involved in inflammation-induced cancer cells proliferation and therefore could be a potential chemopreventive agent against inflammation-associated colon cancer.
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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.