## 3 Results
### Molecular Docking  
Due to the high inhibitory capability, the compounds abundant in the extract of _P. cauliflora_ were analyzed to determine the possible binding/inhibition modes via the docking studies. Based on the GC-MS analysis (Table 1), the top 3 compounds (>6.0%), namely 5-hydroxymethylfurfural, 2,3-dihydro-3,5-dihydroxy-6-methyl-4-pyran-4-one, and 2,5-diformylfuran, were used for docking analysis. The binding mode of these compounds  
Figure 7: The extract of _P. cauliflora_ inhibited the cell migration. (**A**) B16F10 cell migration was analyzed after a 24-h incubation with the _P. cauliflora_ extract using the wound healing assay. The dashed lines indicate the wound edges. The _P. cauliflora_ extract (1500 ug/mL) completely inhibited B16F10 cell migration. (**B**) The wound healing area was quantified, and the results showed that after 24 h of incubation, the _P. cauliflora_ extract at concentrations of 400, 800, 1000, and 1500 ug/mL reduced B16F10 cell migration by 15%, 36%, 75%, and 100%, respectively. The error bars represent the standard deviation, calculated from three independent measurements. As a control group, B16F10 cells were incubated with the culture medium containing 0.2% DMSO. \({}^{**}\)_p_ < 0.01 and \({}^{***}\)_p_ < 0.001 compared with the control group. to KpSSB was elucidated using the MOE Dock tool (Figure 9). Previously, we solved the crystal structure of KpSSB. The structure of KpSSB (Figure 9A) was therefore used for this docking analysis. KpSSB is a monotteramer. Given that the ssDNA-complexed structure of KpSSB is unavailable, the structure of _P. aeruginosa_ SSB (PaSSB) bound by ssDNA dT25 (PDB ID 6 IRQ) was used for analysis (Figure 9B). Bound ssDNA in PaSSB was found to adopt an S-shaped conformation (Figure 9B). Considering their structural similarity, the ssDNA-binding mode between KpSSB and PaSSB may be similar (Figure 9C). According to the docking results (Figure 9C), 5-hydroxymethylfurfural (Figure 9D), 2,3-dihydro-3,5-dihydroxy-6-methyl-4h-pyran-4-one (Figure 9E), and 2,5-diformylfuran (Figure 9F) occupy the ssDNA-binding sites of KpSSB. Thus, these compounds may influence the ssDNA-binding activity of KpSSB by this inhibition mechanism. The binding energies of these compounds were also calculated by MOE (Table 2). The predicted binding affinities for these KpSSB complexes were calculated for all potential binding geometries. Their docking scores revealed the following order for binding affinity (the 5 score): 5-hydroxymethylfurfural > 2,5-diformylfuran > 2,3-dihydro-3,5-dihydroxy-6-methyl-4h-pyran-4-one. The compound 5-hydroxymethylfurfural may possess the greatest binding affinity for KpSSB among the selected compounds, as indicated by the highest 5 score (\(-\)4.3646). However, this conjecture requires further experimental and structural investigations to be confirmed. Figure 8: The extract of _P. caulflora_ inhibited the cell proliferation. (**A**) Estimation of the proliferation of B16F10 cells using the clonogenic assay. The _P. caulflora_ extract (1500 \(\mu\)g/mL) almost completely suppressed the colony formation. (**B**) The quantified results of the proliferation of B16F10 cells are presented. The _P. caulflora_ extract at concentrations of 400, 800, 1000, and 1500 \(\mu\)g/mL significantly inhibited the proliferation of B16F10 cells by 8%, 29%, 69%, and 96%, respectively. The error bars represent the standard deviation from 3 independent measurements. As a control group, B16F10 cells were incubated with the culture medium containing 0.2% DMSO. ** \(p\) < 0.01 and *** \(p\) < 0.001 compared with the control group. Figure 9: The docking studies. (**A**) Crystal structure of KpSSB. KpSSB is a homotetramer with subunits A, B, C, and D. The binding mode of (1) 5-hydroxymethylfurfurral (light magenta), (2) 2.3-dihydro-3,5-dihydroxy-6-methyl-4h-pyran-4-one (cyan), and (3) 2,5-diformylfuran (slate) to KpSSB was elucidated using the MOE Dock tool. (**B**) The structure of PaSSB bound by ssDNA dT25.