Identification of Growth Factors, Cytokines and Mediators Regulated by Artemisia annua L. Polyphenols (pKAL) in HCT116 Colorectal Cancer Cells: TGF-β1 and NGF-β Attenuate pKAL-Induced Anticancer Effects via NF-κB p65 Upregulation
| Autor: | Eun Joo Jung, Anjugam Paramanantham, Hye Jung Kim, Sung Chul Shin, Gon Sup Kim, Jin-Myung Jung, Soon Chan Hong, Ky Hyun Chung, Choong Won Kim, Won Sup Lee |
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| Jazyk: | angličtina |
| Rok vydání: | 2022 |
| Předmět: |
QH301-705.5
Organic Chemistry colorectal cancer General Medicine antibody array Catalysis Computer Science Applications Inorganic Chemistry Artemisia annua L. polyphenols Chemistry TGF-β1 cytokine anticancer effect NGF-β NF-κB p65 Physical and Theoretical Chemistry Biology (General) Molecular Biology QD1-999 Spectroscopy |
| Zdroj: | International Journal of Molecular Sciences, Vol 23, Iss 1598, p 1598 (2022) International Journal of Molecular Sciences; Volume 23; Issue 3; Pages: 1598 |
| ISSN: | 1661-6596 1422-0067 |
| Popis: | The anticancer effects of natural phytochemicals are relevant to the modulation of cytokine signaling pathways in various cancer cells with stem-like properties as well as immune cells. The aim of this study was to elucidate a novel anticancer mechanism of Artemisia annua L. polyphenols (pKAL) involved in the regulation of growth factors, cytokines and mediators in stem-like HCT116 colorectal cancer cells. Through RayBiotech human L-1000 antibody array and bioinformatics analysis, we show here that pKAL-induced anticancer effects are associated with downregulation of growth factor and cytokine signaling proteins including TGFA, FGF16, PDGFC, CCL28, CXCR3, IRF6 and SMAD1. Notably, we found that TGF-β signaling proteins such as GDF10, ENG and TGFBR2 and well-known survival proteins such as NGF-β, VEGFD and insulin were significantly upregulated by pKAL. Moreover, the results of hematoxylin staining, cell viability assay and Western blot analysis demonstrated that TGF-β1 and NGF-β attenuated pKAL-induced anticancer effects by inhibiting pKAL-induced downregulation of caspase-8, NF-κB p65 and cyclin D1. These results suggest that certain survival mediators may be activated by pKAL through the TGF-β1 and NGF-β signaling pathways during pKAL-induced cell death and thus, strategies to inhibit the survival signaling are inevitably required for more effective anticancer effects of pKAL. |
| Databáze: | OpenAIRE |
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