This study explored the effect of different concentrations of lapatinib (from 3.125 to 50 μM) on biofilm formation of S. Therefore, we sought to explore the characteristics and mechanisms behind this lapatinib-induced inhibition of growth, biofilm formation, and hemolytic activity of S. Interestingly, our preliminary experiments showed that lapatinib inhibits the biofilm formation of S. Inspired by these studies, we explored the effects of lapatinib on the growth and biofilm formation of S. (14) showed that lapatinib is a strong promoter of Francisella novicida biofilm formation. (12) It was discovered that lapatinib inhibited multiplication of Mycobacterium spp. (11) Lapatinib is mainly used in combination with capecitabine to treat advanced or metastatic breast cancer with ErbB2 overexpression. (10) Lapatinib induces cell cycle arrest and promotes cell apoptosis through inhibition of the MAPK and PI3K/Akt downstream signaling pathways, resulting in an antitumor effect. Lapatinib is an orally effective quinazoline derivative that inhibits epidermal growth factor receptors 1 (ErbB1) and 2 (ErbB2) in human cells.
In conclusion, this study indicates that lapatinib significantly inhibits biofilm formation and the hemolytic activity of S. We identified four genes with mutations: three genes with known functions (membrane protein, pyrrolidone-carboxylate peptidase, and sensor histidine kinase LytS, respectively) and one gene with unknown function (hypothetical protein). aureus isolates with reduced susceptibility to lapatinib were detected by whole-genome sequencing. aureus isolates was significantly weakened) were selected. aureus isolates with reduced susceptibility to lapatinib (the inhibitory effect of lapatinib on the biofilm formation of these S. aureus isolates were continuously cultured in vitro in the presence of increasing concentrations of lapatinib for about 140 days. aureus decreased after 6 h treatment with lapatinib. Using quantitative reverse transcription PCR, we found that the RNA levels of transcriptional regulatory genes ( RNAIII, agrA, agrC, saeR, and saeS), biofilm-formation-related genes ( atl, cidA, clfA, clfB, and icaA), and virulence-related genes ( cap5A, hla, hld, hlg, lukDE, lukpvl-S, staphopain B, alpha-3 PSM, beta PSM, and delta PSM) of S. aureus (MSSA) and methicillin-resistant S. Herein, we show that lapatinib (12.5 μM) significantly inhibits biofilm formation and hemolytic activity of both methicillin-sensitive S. Biofilm formation and hemolytic activity are closely related to the pathogenesis of Staphylococcus aureus infections.
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