Fig. 6

Functional complementarity experiments demonstrated that METTL3 regulates METTL4-2 expression in CSCC progression. We firstly constructed C33A cells transfected with Sh-NC, lncRNA METTL4-2 OE, Sh-METTL3#1, and lncRNA METTL4-2 OE+Sh-METTL3#1 treatment, respectively. In animal experiments, we inoculated C33A cells performed with the above treatments subcutaneously at the armpits of mice. A Cell viability of C33A cells was measured by CCK-8 assay (n=3). B Colony formation assays of C33A cells (n=3). C The invasion of C33A cells was assessed by transwell assay (n=3). D The migration of C33A cells of indicated treatment was assessed by wound healing assay (n=3). E The levels of E-cadherin, N-cadherin, vimentin, and FN1 in C33A cells were detected by western blot (n=3). F Typical CSCC tumors from mice after subcutaneous injection of C33A cells with different treatments (n=4). G Tumor volume was measured every week by growth curve (n=4). H Tumor weight was measured at the end of experiments (at the 5 weeks) (n=4). *p < 0.05; **p < 0.01; ***p < 0.001