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• W2893699686 abstract "IFN-λs are a kind of cytokine with anti-tumor, immunomodulatory, and anti-proliferative activity. Recent studies have shown that the recombinant Newcastle disease virus expresses human IFN-λ1 (rL-hIFN-λ1), which plays a role in gastric cancer cell apoptosis. Endoplasmic reticulum stress (ERS) induces autophagy and apoptosis in tumor cells. In this study, we explored the relationship between ERS and rL-hIFN-λ1-induced apoptosis of lung adenocarcinoma A549 cells and its underlying mechanism.First, we investigated the effect of rL-hIFN-λ1 on cellular proliferation, migration, and proteins associated with ERS, autophagy, and apoptosis of A549. Second, after administration of the ERS inhibitor, the associated proteins induced by rL-hIFN-λ1 were detected. Finally, a subcutaneous mouse model was used to examine the effect of rL-hIFN-λ1 on tumor growth and the ERS and apoptosis associated proteins in tumor tissues.The results showed that the proliferation and migration of A549 cells, and tumor tissue growth were significantly inhibited and the ERS, autophagy, and apoptosis associated proteins were upregulated in the experimental group. Additionally, both 4-PBA and knockdown of PERK or CHOP reduced the levels of rL-hIFN-λ1-induced autophagy and apoptosis-associated proteins. BCL-2 knockdown caused autophagy and apoptosis associated protein upregulation.In summary, rL-hIFN-λ1 inhibited cell proliferation and activated ERS, autophagy, and apoptosis in A549 cells and tissues, and when ERS pathways were blocked, the inhibiting effect was even more pronounced. Therefore, the recombinant Newcastle disease virus rL-hIFN-λ1-induced apoptosis of A549 cells is connected to ER stress and could be a promising therapeutic agent for lung adenocarcinoma." @default.
• W2893699686 created "2018-10-05" @default.
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• W2893699686 date "2018-09-23" @default.
• W2893699686 modified "2023-10-16" @default.
• W2893699686 title "Recombinant Newcastle disease virus expressing human IFN-λ1 (rL-hIFN-λ1)-induced apoptosis of A549 cells is connected to endoplasmic reticulum stress pathways" @default.
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• W2893699686 doi "https://doi.org/10.1111/1759-7714.12857" @default.
• W2893699686 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6209783" @default.
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• W2893699686 hasPublicationYear "2018" @default.
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