Bufalin\'s Pro Government Adenocarcinoma Molecular and Metab | 97300
International Research Journals

Bufalin\'s Pro Government Adenocarcinoma Molecular and Metabolic Mechanisms: Fresh and Detailed Data from Network Pharmacology, Metabolomics, and Molecular Biology Investigations


Shrishtika Singh*

By a thorough approach incorporating network pharmacology, metabolomics, and molecular biology verification, this study seeks to assess the therapeutic efficacy and mechanism of bufalin on lung cancer. The Swiss Target Prediction database and Pharm Mapper were used to identify the possible targets of bufalin. Target filtering of the Gene Card database and data mining of the GEO database were used to find LUAD-related targets. The core targets were screened using a PPI network, and the clinical importance of each target was evaluated using a number of open databases. To find potential enrichment of genes with particular biological topics, GO and KEGG pathway studies were carried out. To ascertain the correlation and binding pattern between bufalin and core targets, molecular docking and molecular dynamics modelling were used. The network-predicted methods via which bufalin affects LUAD In-vitro and in-vivo models were used to experimentally validate the pharmacological analyses. Finally, non-targeted metabolomics was used to examine how bufalin intervention affected the metabolite profile and metabolic pathway in LUAD nude mice. 51 junction targets were found among the 1082 LUAD-associated and bufalin targets that were extracted. Using network topology analysis, 10 main targets, including Akt1, STAT3, EGFR, CASP3, and SRC, were identified. Molecular docking and MD simulations revealed that these targets exhibited a strong affinity for bufalin. Cell proliferation and death were tightly correlated with the hub module of the PPI network. Bufalin was found to be effective in treating LUAD by suppressing proliferation and inducing apoptosis via the PI3K/Akt, FoxO1, and MAPK/ERK pathways, as revealed by GO and KEGG enrichment analyses. This was supported by a number of subsequent studies. Of in-vitro research and the tumour tissues' HE, TUNEL, and Ki-67 staining. Bufalin largely controlled ABC transporter regulation and altered AA metabolism, which helped treat LUAD, according to further metabolomics study. The current study, which successfully filtered out associated key target genes, differential endogenous metabolites, and signalling pathways, not only provided a unique insight into the potential mechanisms of bufalin against LUAD from a molecular and metabolic perspective, but also suggested a novel, promising therapeutic approach for LUAD.

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