Corrigendum: Network pharmacology-based exploration identified the antiviral efficacy of Quercetin isolated from mulberry leaves against enterovirus 71 via the NF-κB signaling pathway.

[This corrects the article DOI: 10.3389/fphar.2023.1260288.].

Integrated Analysis Construct a Tumor-Associated Macrophage Novel Signature with Promising Implications in Predicting the Prognosis and Immunotherapeutic Response of Gastric Cancer Patients.

BACKGROUND: Gastric cancer (GC) remains one of the most prevalent malignant tumors worldwide. At present, tumor-associated macrophages (TAMs) are essential in the progression, metastasis, and drug resistance of tumors. Therefore, TAMs can be a crucial target for tumor treatment. AIMS: We intended to investigate the TAM characteristics in GC and develop a risk signature based on TAM to predict the prognosis of GC patients. METHODS: The single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data were acquired from a publicly available database. We utilized the Seurat pipeline to process the scRNA-seq data and determine TAM cell types using marker genes. Univariate Cox regression analysis was utilized to examine TAM-related prognostic genes, and then we employed Lasso-Cox regression analysis, and Multivariate Cox regression analysis established a novel risk profile to forecast the clinical value of the model with a new nomogram combining risk profiles and clinicopathological characteristics. RESULTS: The current study employed scRNA-seq data to identify five TAM clusters in GC, among which four were significantly associated with GC prognosis. Accordingly, we further developed a TAM-related risk signature utilizing nine genes. After evaluation, our model accurately predicted the prognosis of gastric cancer. Generally, GC patients with low TAMS scores exhibited a more favorable prognosis, greater benefits from immunotherapy, and higher levels of immune cell infiltration. CONCLUSIONS: The prognosis of GC can be effectively predicted by TAM-based risk signatures, and the signature may provide a new perspective for comprehensively guiding clinical diagnosis, prediction, and immunotherapy for gastric cancer.

Network pharmacology-based exploration identified the antiviral efficacy of Quercetin isolated from mulberry leaves against enterovirus 71 via the NF-κB signaling pathway.

Introduction: Mulberry leaf (ML) is known for its antibacterial and anti-inflammatory properties, historically documented in "Shen Nong's Materia Medica". This study aimed to investigate the effects of ML on enterovirus 71 (EV71) using network pharmacology, molecular docking, and in vitro experiments. Methods: We successfully pinpointed shared targets between mulberry leaves (ML) and the EV71 virus by leveraging online databases. Our investigation delved into the interaction among these identified targets, leading to the identification of pivotal components within ML that possess potent anti-EV71 properties. The ability of these components to bind to the targets was verified by molecular docking. Moreover, bioinformatics predictions were used to identify the signaling pathways involved. Finally, the mechanism behind its anti-EV71 action was confirmed through in vitro experiments. Results: Our investigation uncovered 25 active components in ML that targeted 231 specific genes. Of these genes, 29 correlated with the targets of EV71. Quercetin, a major ingredient in ML, was associated with 25 of these genes. According to the molecular docking results, Quercetin has a high binding affinity to the targets of ML and EV71. According to the KEGG pathway analysis, the antiviral effect of Quercetin against EV71 was found to be closely related to the NF-κB signaling pathway. The results of immunofluorescence and Western blotting showed that Quercetin significantly reduced the expression levels of VP1, TNF-α, and IL-1ß in EV71-infected human rhabdomyosarcoma cells. The phosphorylation level of NF-κB p65 was reduced, and the activation of NF-κB signaling pathway was suppressed by Quercetin. Furthermore, our results showed that Quercetin downregulated the expression of JNK, ERK, and p38 and their phosphorylation levels due to EV71 infection. Conclusion: With these findings in mind, we can conclude that inhibiting the NF-κB signaling pathway is a critical mechanism through which Quercetin exerts its anti-EV71 effectiveness.