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cas2302-sup-0001-FigS1-S11.docWord document399KFig. S1. The correlation between dysadherin and phospho-AKT (pAKT) expression in breast cancer tissues. Fig. S2. Cell viability analysis in breast cancer cell lines. Fig. S3. Immunoblot analysis of dysadherin in MCF-7 cells after transfection with mock (empty vector) or Dys (Dysadherin cDNA) following 48 h treatment with 100 nM triciribine. Fig. S4. qRT-PCR analysis of E-cadherin in MCF-7 cells after transfection with mock (empty vector) or Dys (Dysadherin cDNA) following 48 h treatment with 1 nM triciribine. Fig. S5. qRT-PCR analysis of CCL2 in MDA-MB-231 and Hs578T cells after 24 h treatment with 100 nM triciribine. Fig. S6. Immunoblot analysis of AKT activity level in MDA-MB-231 cells after transfection with shCon (control shRNA) or shDys (Dysadherin shRNA) following 24 h treatment with recombinant CCL2 protein (R&D Systems, Minneapolis, MN, USA; 100 ng/mL). Fig. S7. Immunoblot analysis of the level of MEK and pMEK after modification of the Dysadherin gene in MCF-7 and MDA-MB-231 breast cancer cell lines. Fig. S8. The effect of Akt inhibition on dysadherin-mediated NF-κB activation. Fig. S9. Immunoblot analysis of AKT activity level in T-47D cells after transfection with mock (empty vector) or Dys (Dysadherin cDNA) following 24 h treatment with 1 μM 6-amino-4-(4-phenoxyphenylethylamino)quinazoline (Calbiochem; NF-κB inhibitor). Fig. S10. Immunoblot analysis of PIK3CA after modification of the Dysadherin gene in breast cancer cell lines. Fig. S11. Immunoblot analysis of AKT activity level in MCF-7 cells after transfection with mock (empty vector) or Dys (Dysadherin cDNA) following 1 h treatment with 10 μM LY294002 (Calbiochem; PIK3CA inhibitor).
cas2302-sup-0002-TableS1.pdfapplication/PDF56KTable S1. Clinicopathological characteristics of breast cancer tissue samples by immunofluorescent analysis.

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