Supplementary Figures 1-13 from Destrin Contributes to Lung Adenocarcinoma Progression by Activating Wnt/β-Catenin Signaling Pathway

Abstract

<p>Supplementary Figure 1. Time-course analysis of the development of lung tumors induced by urethane in BALB/C mice and MS/MS analysis of destrin identified. Supplementary Figure 2. Validation of targeted proteins chosen by immunohistochemistry analysis. Supplementary Figure 3. Protein expression levels of Prdx5, Ctsd, Ctsh, Ctnna1, and Jup with reference to GAPDH (internal control), examined by immunoblot in the lung tissues of normal control mice and the mice at week 16 and 32 after Urethane treatment. Supplementary Figure 4. The effect of DSTN knockdown or overexpression on colony formation and migration in BEAS-2B cells. Supplementary Figure 5. Representative images of IHC staining using Ki67. Supplementary Figure 6. DSTN knockdown induces G2/M phase arrest in A549 and H1299 cells. Supplementary Figure 7. DSTN knockdown promotes apoptosis in A549 and H1299 cells. Supplementary Figure 8. The effect of DSTN knockdown or overexpression on the migration of A549 and H1299 in vitro. Supplementary figure 9. The effect of DSTN knockdown or overexpression on anchorage-independent growth of A549 and H1299 in vitro. Supplementary figure 10. The effect of DSTN knockdown or overexpression on EMT marker expression. Supplementary Figure 11. The effect of DSTN knockdown or overexpression on the adhesive ability of the A549 and H1299 cells. Supplementary Figure 12. DSTN knockdown or overexpression affects the sub-cellular localization of β-catenin in A549 and H1299 cells. Supplementary figure 13. The interaction between DSTN and β-catenin was assessed by Co-immunoprecipitation.</p>