Background　The　global　epidemiological　studies　reported　lower　cancer　risk　after　long-term　use　of　contraceptives.　Our　systematic　studies　demonstrated　that　abortifacients　are　effective　in　preventing　cancer　metastases　induced　by　circulating　tumor　cells　(CTCs).　However,　the　molecular　and　cellular　mechanisms　by　which　abortifacients　prevent　CTC-based　cancer　metastases　are　almost　unknown.　The　present　studies　were　designed　to　interdisciplinarily　explore　similarities　and　differences　between　embryo　implantation　and　cancer　cell　adhesion/invasion.　Methods　Biomarker　expressions　on　the　seeding　embryo　JEG-3　and　cancer　MCF-7　cells,　as　well　as　embedding　uterine　endometrial　RL95-2　and　vascular　endothelial　HUVECs　cells　were　examined　and　compared　before　and　after　treatments　with　17　beta-estradiol　plus　progesterone　and　abortifacients.　Effects　of　oral　metapristone　and　mifepristone　on　embryo　implantation　in　normal　female　mice　and　adhesion/invasion　of　circulating　tumor　cells　(CTCs)　in　BALB/C　female　mice　were　examined.　Results　Both　embryo　JEG-3　and　cancer　MCF-7　cells　expressed　high　sLex,　CD47,　CAMs,　while　both　endometrial　RL95-2　and　endothelial　HUVECs　exhibited　high　integrins　and　ICAM-1.　Near　physiological　concentrations　of　17　beta-estradiol　plus　progesterone　promoted　migration　and　invasion　of　JEG-3　and　MCF-7　cells　via　upregulating　integrins　and　MMPs.　Whereas,　mifepristone　and　metapristone　significantly　inhibited　migration　and　invasion　of　JEG-3　and　MCF-7　cells,　and　inhibited　JEG-3　and　MCF-7　adhesion　to　matrigel,　RL95-2　cells　and　HUVECs,　respectively.　The　inhibitions　were　realized　by　downregulating　sLex,　MMPs　in　JEG-3　and　MCF-7　cells,　and　downregulating　integrins　in　RL95-2　cells　and　HUVECs,　respectively.　Mifepristone　and　metapristone　significantly　inhibited　both　embryo　implantation　and　cancer　cell　metastasis　in　mice.　Conclusions　The　similarities　between　the　two　systems　provide　fundamentals　for　abortifacients　to　intervene　CTC　adhesion/invasion　to　the　distant　metastatic　organs.　The　present　studies　offer　the　rationale　to　repurpose　abortifacients　for　safe　and　effective　cancer　metastasis　chemoprevention.