Fig. 1

Tumor formation is delayed in basal-like Brca1/p53-deficient tumors lacking Itga6. A In silico analysis of ITGA6 mRNA expression in human breast cancer subtypes classified by the PAM50 signature: Normal-like (n = 8), Luminal A (n = 231), Luminal B (n = 127), HER2-enriched (n = 58), and basal-like (n = 98). B Kaplan–Meier tumor-free survival curve of Brca1p53-KO (n = 56) α6 ± ;Brca1p53-KO (n = 19) and α6KO/Brca1p53-KO (n = 44) females. P = 0.13 (Brca1p53-KO vs. α6 ± ;Brca1p53-KO); P = 0.0001 (Brca1p53-KO vs. α6KO/Brca1p53-KO); P = 0.001 (α6 ± ;Brca1p53-KO vs. α6KO/Brca1p53-KO). C Number of mammary tumors per mouse in Brca1p53-KO (n = 55) α6 ± ;Brca1p53-KO (n = 11) and α6KO/Brca1p53-KO (n = 43) females. D, E Histological analysis of Brca1p53-KO and α6KO/Brca1p53-KO tumors. D Hematoxylin/eosin staining. E Immunofluorescent staining with anti-PR (red), anti-K8 (white) and anti α-SMA (green) antibodies. Nuclear DAPI staining is shown in blue. In the tumors, α-SMA staining is mostly restricted to tumor fibroblast. White arrows indicate the presence of normal ductal luminal cells positively stained for PR. Scale bar: 100 µm (D) and 20 µm (E). In A, C: *P < 0.05, ****P < 0.0001, n.s., non-significant