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. Author manuscript; available in PMC: 2017 Mar 15.
Published in final edited form as: Cancer Res. 2016 Jan 12;76(6):1451–1462. doi: 10.1158/0008-5472.CAN-15-1941

Figure 1. AKT genes signature co-regulated by EMT discriminates basal-like versus luminal subtype of breast cancers.

Figure 1

(A) Nonsupervised clustering of 54 breast cancer cell lines based on 10 genes. Gene expression heat map showing distinct expression pattern between basal- and luminal-breast cancer cell lines. TNBC gene signatures ESR1, ERBB2 and PgR are included.

(B) Box plots showing the average expression level of AKT1/2/3 or individual AKT isoforms gene in basal and luminal breast cancer cell lines (left) and (middle) from (A). Gene expression expressed as epithelial/mesenchymal ratio is shown (right).

(C and D) Box plots showing the average expression level of AKT1/2/3 (left), AKT1, AKT2 andAKT3 (middle and right) in basal and luminal cancers of NCI cohort (C) and of UNC cohort (D).

(E) Luciferase reporter assay of HEK-293 cells were transfected with the E-cadherin reporter together with increasing amount of myr-AKT1, myr-AKT2 or myr-AKT3.

(F) Gene expression heat map of E-cadherin, EPCAM, N-cadherin and vimentin in MDA-MB-231 cells expressing the myr-AKT isoforms.

(G) Kaplan-Meier analysis of p-AKT 473 survival of breast cancer patients in the MD Anderson Cancer Center cohort.

(H) Kaplan-Meier analysis of AKT1 by stratifying patients with quartiles partition.