Fig. 6

IGF2BP3 was involved in m6A methylation modification in LSCC. a RIP-qPCR was showing the enrichment of IGF2BP3 binding to TMBIM6 m6A modification sites. b and c After knocked down or overexpressed IGF2BP3, qRT-PCR evaluated the expression of IGF2BP3 in LSCC cells. d and e MeRIP assays were performed to identify variation in m6A modification enrichment in TMBIM6 after silencing or overexpressing IGF2BP3 in LSCC cells. f and g qRT-PCR of TMBIM6 mRNA after IGF2BP3 inhibition or overexpression in LSCC cells. h RIP-qPCR unveiled the interaction within IGF2BP3 and TMBIM6 mRNA after RBM15 inhibition. i The luciferase activities in AMC-HN-8 cells co-transfected with TMBIM6-WT or TMBIM6-Mut together with shCtrl or shIGF2BP3. j The luciferase activities in TU-212 cells co-transfected with TMBIM6-WT or TMBIM6-Mut together with Vector or IGF2BP3. k qRT-PCR was used to detect IGF2BP3 expression in 34 pairs of LSCC tissues. l Results based on the TCGA and GEPIA databases showed the expression level of IGF2BP3 in HNSC. m IHC staining of IGF2BP3 in LSCC tumour specimens. n Kaplan-Meier survival analysis showed that the expression level of IGF2BP3 in LSCC patients was significantly related to the OS. o and p Data from the TCGA database showed that the expression level of IGF2BP3 in HNSC patients was significantly related to OS and RFS. q Correlation analysis was conducted on the expression levels of TMBIM6 and IGF2BP3 in 34 cases of LSCC tissues. r Correlation analysis was performed on the expression levels of TMBIM6 and IGF2BP3 in the TCGA database