Fig. 3

A PCR detection confrmed that LCN2 was successfully inhibited in the EGFR-resistant OSCC cell lines. B Western blotting confrmed that LCN2 was successfully inhibited in CAL-27ER and HN-6ER cells. C and D After the expression of LCN2 was downregulated, the migration and invasion of CAL-27ER cells were signifcantly inhibited, and the cells that passed through the upper chamber of the Transwell were signifcantly reduced. (Scale bar: 100 μm). E The scratch test showed that LCN2 was downregulated, the migration function of CAL-27ER cells was signifcantly downregulated, and the scratch healing speed (recovery rate) was decreased. F The cell colony formation test showed that after inhibiting LCN2 in ER-resistant cells, the colony formation of OSCC cells decreased signifcantly. G and H Inhibiting the expression of LCN2 signifcantly decreased the proliferation ability of OSCC cells, and the CCK-8 results were lower than those of the control group. I PCR detection confrmed that LCN2 was successfully overexpressed in wild-type CAL-27 and HN-6 cells. J Western blotting showed that LCN2 was successfully overexpressed in wild-type CAL-27 and HN-6 cells. K and L After overexpression of LCN2, the migration and invasion of CAL-27 cells were signifcantly upregulated, and the number of cells that passed through the upper chamber of the Transwell was signifcantly increased. (Scale bar: 100 μm). M After the scratch experiment confrmed that LCN2 was overexpressed, the migration ability of CAL-27 cells was signifcantly upregulated, and the scratch healing speed was increased. N The cell colony formation assay showed that the colony formation of OSCC cells increased signifcantly when LCN2 was overexpressed. O and P Upregulation of LCN2 in OSCC cells signifcantly increased their proliferation abilities, and the CCK-8 values were higher than those of the control group