TIMP2, MMP2 and CD63 as shared molecular mediators of embryo implantation, endometriosis and cancer metastasis: a transcriptomic hypothesis

Malignant tumors do not create fundamentally new cellular mechanisms - to achieve invasive growth and metastasis, they exploit programs already encoded in the genome. We propose the hypothesis that embryo implantation, endometriosis, and cancer metastasis share a common molecular mechanism of adhesive invasion. To test this hypothesis, we performed a comparative bioinformatic analysis of three independent transcriptomic datasets from the NCBI GEO database: GSE7305 (endometriosis vs normal endometrium, n=20), GSE111974 (recurrent implantation failure vs normal fertility, n=48), and GSE17536 (colorectal cancer stage 3-4 vs stage 1-2, n=177). The analysis revealed a consistent gene expression pattern: TIMP2, MMP2, and CD63 are upregulated in endometriosis and metastatic cancer, and downregulated in recurrent implantation failure. TIMP2 is the only gene significantly altered in both pathological contexts (p<0.0001 and p=0.015). These findings support the concept that pathological reactivation of the physiological implantation program underlies both endometriosis and cancer metastasis, and identify TIMP2 as a priority candidate for functional investigation and therapeutic targeting.