{"paper_id":"a2740add-2003-47ae-910c-955bdaddde27","body_text":"TIMP2, MMP2 and CD63 as shared molecular mediators of embryo implantation, endometriosis and cancer metastasis: a transcriptomic hypothesis\nAuthors/Creators\nDescription\nMalignant 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.\nFiles\nFiles\n(14.7 kB)\n| Name | Size | Download all |\n|---|---|---|\n|\nmd5:618d02ba7bf7a536638f5094bf4b5444\n|\n14.7 kB | Download |","source_license":"CC0","license_restricted":false}