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Archive > Volume 32 Issue 9 > 2025,32(9):934-940. DOI:10.3872/j.issn.1007-385X.2025.09.006 Prev Next
Basic Research
Echinatin inhibits malignant behaviors and immune escape of lung cancer A549 cells by activating the STING/TBK1/IRF3 signaling pathway
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Abstract:
[Abstract] Objective: To investigate the effects of echinatin (Ech) on the malignant biological behavior and immune escape of lung cancer A549 cells and its underlying mechanisms. Methods: Normal lung epithelial cells (BEAS-2B) and A549 cells were routinely cultured and treated with different concentrations of Ech for 24h. Cell viability was assessed using the MTT assay, and concentrations of 20, 30, and 40 μmol/L were selected for subsequent experiments. A549 cells were divided into the following groups: control group (0 μmol/L Ech), low- (20 μmol/L), medium- (30 μmol/L), and high-concentration (40 μmol/L) Ech groups (Ech-L, Ech-M, Ech-H), and high-dose Ech combined with the pathway inhibitor H-151 (1.0 μmol/L) group (Ech-H + H-151). Cell proliferation, migration, and invasion were evaluated using the EdU assay, wound-healing assay, and Transwell assay, respectively. Western blotting (WB) assay was applied to detect the expression of proteins related to proliferation, migration, invasion, and the STING/TBK1/IRF3 signaling pathway. Subsequently, A549 cells were co-cultured with CD8+ T cells, and trypan blue staining was used to detect CD8+ T cell viability. The levels of type Ⅰ interferon (IFN-Ⅰ) in the co-culture supernatants were detected by WB, while the levels of programmed death ligand 1 (PD-L1), interleukin-10 (IL-10), interleukin-4 (IL-4), and transforming growth factor-β (TGF-β) were determined using ELISA. Results: Ech inhibited the viability of A549 cells in a dose-dependent manner (all P < 0.05) but had no significant effect on the viability of BEAS-2B cells. Ech dose-dependently inhibited the proliferation, migration and invasion of A549 cells (all P < 0.05), as well as the protein expression of cyclinD1, Ki67, MMP2, MMP9, STING, p-TBK1 and p-IRF3 (all P < 0.05). These effects were partially reversed by H-151. Ech dose-dependently promoted the survival of CD8+ T cells co-cultured with A549 cells (all P < 0.05), enhanced IFN-Ⅰ expression (all P < 0.05), and inhibited the secretion of PD-L1, IL-10, IL-4, and TGF-β (all P < 0.05), with H-151 partially reversing these effects (all P < 0.05). Conclusion: Ech inhibits malignant biological behavior and immune escape of lung cancer A549 cells by activating the STING/TBK1/IRF3 signaling pathway.
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