Fig. 6

The MALAT1-KTN1-EGFR regulatory axis exists in vivo. MALAT1 ASO were injected into A431 cell xenografts every 2 days. a Loss of MALAT1 attenuates subcutaneous tumor growth in a mouse xenograft model. Tumor volumes (mm³) were plotted according to days. Tumor volumes statistical data represent the average of five independent experiments ± s.d, respectively. b The mice were sacrificed at the end of the experiment and images taken along with the dissected tumors from five representative mice are shown. Black arrows indicate NC ASO-treated xenografts while white arrows indicate MALAT1 ASO-treated xenografts. c The expression of MALAT1 in the dissected tumors was measured by qRT-PCR. qRT-PCR statistical data represent the average of three independent experiments ± s.d, respectively. d The protein expression of KTN1 and EGFR was detected in the xenografts. e RNA in situ hybridization assay was used to detect expression of MALAT1 in NC and MALAT1 ASO-treated xenografts. Scale bar, 50 µm. f Histopathology analysis (IHC staining) showing the marked loss of the expression of EGFR and KTN1 in xenografts. Scale bar, 100 µm. *P < 0.05, **P < 0.01, ***P < 0.001. g The model depicts the roles of the MALAT1-KTN1-EGFR regulatory axis. In cSCC tumors, the aberrantly expressed MALAT1 interacts with c-MYC to form a complex, binds to the promoter region of KTN1 gene and transcriptionally enhances KTN1 expression. The upregulated KTN1 may associate with protein translation machine to promote EGFR expression at the protein level, which contributes to cSCC development