Fig. 1: E-cadherin is a crucial hub in oestrogen-mediated cancer responses with sex-dependent effects on melanoma metastasis.
From: Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin

a,b, Incidence ratios (women/men) for all cancers (a) and malignant melanoma of the skin (b) across different age groups, depicted as age-standardized rates (ASR). Data sourced from GLOBOCAN 2020 (ref. 6). c, Plasmatic oestradiol concentration stratified by age and sex. d, Venn diagram highlighting the overlap between genes associated with cancer, demonstrating a peak in incidence in women aged 15–55 (with melanoma, breast cancer, thyroid cancer and gastric cancer) and genes associated with ESR1. The four indicated genes are at the intersection of all five categories. e, Expression of CDH1, CCND1, BRAF and KRAS in human melanoma (TCGA database) stratified by sex and age. TPM, transcripts per million reads. f, Kaplan–Meier survival curves for melanoma-free mice categorized by E-cadherin status and sex; n is the number of mice per condition. No significant differences were observed by log-rank analysis. g,h, Representative lung images from female mice with primary melanoma for Ecad (g) or mutated Ecad (h). Yellow hexagons, micro-metastases; white circles, macro-metastases; scale bar, 2 mm; g and h are at the same scale. i, Frequency of lung metastasis in mice categorized by Ecad and sex status. j, Metastasis quantification based on Ecad and sex status. Significance was assessed by chi-square test for metastasis proportions and two-sided Mann–Whitney test adjusted for multiple testing by the Benjamini–Hochberg method for metastasis counts. NS, not significant.