ReferenceID 1161
Icaritin ameliorates extracellular microparticles-induced inflammatory pre-metastatic niche via modulating the cGAS-STING signaling
Phytother Res
The concept of the inflammatory pre-metastatic niche (PMN) provides a new and promising direction for the prevention and treatment of metastasis. The excessive activation of the GAS-STING signaling leads to augmented met
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Record Fields
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- Reference Id
- 1161
- Evidence Id
- 17751
- Core Evidence Id
- 17751
- Source Reference Id
- 2300
- Herb2 Reference Id
- HBREF003097
- Subject Paper Key
- HBIN016163_35257426
- Pubmed Id
- 35257426
- Doi
- 10.1002/ptr.7433
- Paper Title
- Icaritin ameliorates extracellular microparticles-induced inflammatory pre-metastatic niche via modulating the cGAS-STING signaling
- Paper Abstract
- The concept of the inflammatory pre-metastatic niche (PMN) provides a new and promising direction for the prevention and treatment of metastasis. The excessive activation of the GAS-STING signaling leads to augmented metastasis by promoting the formation of the inflammatory PMN. In this study, tumor-derived microparticles (MP) were used to establish the PMN model both in vitro and in vivo, and pro-inflammatory mediators were also employed to evaluate the effects of Icaritin (ICT). It was demonstrated that ICT could inhibit the pulmonary metastasis of B16BL6 melanoma cells in mice via interfering with PMN. The phosphorylation and dimerization of STING and its downstream signaling TBK1-IFNβ were proved to be diminished in the presence of ICT. Furthermore, we revealed that ICT suppressed the generation of pro-inflammatory PMN through conferring the inactivation of the STING signaling pathway. CETSA and DARTS assay also confirmed that STING tended to be a target for the action of ICT. Collectively, our findings highlight a new binding mechanism between STING and ICT for the inhibition of transduction of the STING signaling pathway, suggesting that pharmacological or therapeutic intervention of the STING-TBK1-IFNβ singling axis may serve as an effective strategy to prevent the progression of inflammatory PMN and lung metastasis.
- Journal
- Phytother Res
- Publish Year
- 2022
- Experiment Subject
- mouse; b16bl6 melanoma cells
- Experiment Type
- Animal Experiment
- Phenotype Related
- B16bl6 Melanoma; Lung Metastasis; Inflammatory Pmn
- Paper Title Cn
- Paper Title En
- Icaritin ameliorates extracellular microparticles-induced inflammatory pre-metastatic niche via modulating the cGAS-STING signaling
- Bilingual Status
- semi_complete