Fig 1: Effects of enolase 1, ubiquitin C, and iTS CM on the expression of tumor-promoting and tumor-suppressing genes. CM = conditioned medium, CN = control (no CM treatment), β-cat = β-catenin plasmids, siEno1 = Enolase 1 siRNA, siUbc = ubiquitin C siRNA, EO = EO771 mammary tumor cells. (A&B) Expression of MMP9, Runx2, Snail, p53, and TRAIL in response to enolase 1 and ubiquitin C in EO771 breast cancer cells. (C&D) Expression of MMP9, Runx2, Snail, p53, and TRAIL in response to β-catenin-overexpressing iTS CM impaired by siRNAs specific to enolase 1 and ubiquitin C. (E) Expression of PDL1 in EO771 mammary tumor cells in response to β-catenin-overexpressing iTS CM, enolase 1, and ubiquitin C. (F&G) Expression of MMP9, Runx2, Snail, p53, TRAIL, and caspase 3 in EO771 mammary tumor cells in response to β-catenin-overexpressing pre-treatment tumor cell-derived CM. (H) Low survival for cancer patients with a high transcript level of MMP9, Runx2, or Snail. (I) Proposed regulatory mechanism to inhibit tumor progression by iTS-CM. According to the mechanism, β-catenin-overexpressing iTS cells secrete ubiquitin C (Ubc), enolase 1 (Eno1), p53, and Trail. They suppress the progression of tumor cells by downregulating MMP9, Runx2, Snail, and PDL1, while upregulating cleaved-caspase 3. It should be noted that Eno1 interacts with CD44 and inhibits MMP9, Runx2, and Snail.