Fig. 8.
a Analysis of CACNA1H (Cav3.2) expression across the intrinsic molecular subtypes of breast cancer in clinical patient samples. The relative CACNA1H expression level (log2 normalised) was produced by the TCGA consortium through RSEM [36]. The TCGA tumour cohort consists of 845 tumours with 140 basal-like (Basal), 67 HER2-enriched (HER2), 420 luminal A (LumA), 194 luminal B (LumB) and 24 normal-like (N-Like) as determined by RNA-Seq based PAM50 allocations by the TCGA consortium. The PAM50 intrinsic molecular subtypes are based on the classifications of gene expression patterns previously described [66, 67]. This classification was performed by the TCGA consortium [35]. Horizontal lines represent data means with standard deviation and data points in grey. Statistical analysis was performed on expression levels of CACNA1H in basal-like compared to HER2-enriched and luminal subtypes using a one-way ANOVA with Sidak corrected multiple comparisons,(****p ≤ 0.0001). b Relative gene expression for breast cancer receptors ERBB2 (HER2), ESR1 (oestrogen receptor) and PGR (progesterone receptor) within each quartile of CACNA1H expression. Statistical analysis was performed using a one-way ANOVA with Sidak corrected multiple comparisons, comparing expression levels between the highest and the lowest quartile for each gene (*p ≤ 0.05, ****p ≤ 0.0001). c Cav3.2 overexpression in SKBR cells (SKBR3 EGFP) did not increase expression of hormone receptors or proteins involved in oestrogen-receptor mediated signalling TFF1, FOXA1, quantified using RT-qPCR. Results are expressed as fold change normalised to EGFP MOCK (n = 3 ±SD)