Furthermore, we observed a mechanistic involvement of miR-200s in this regulation of EMT by PGI/AMF, where overexpression of miR-200s was found to reverse the PGI/AMF-induced EMT and, conversely, silencing of miR-200s was found to induce EMT even in the PGI/AMF-silenced breast cancer cells. Here, GPI is linked to breast cancer.