The present invention relates to a composition for inhibiting cancer metastasis using apoptotic cells, and more specifically, a conditioned medium is prepared by co-culturing macrophages and killed cells, -β1 inhibited the EMT migration and permeation of 344SQ cells. As a result, it was confirmed that EMT, migration and penetration inhibition were also observed in A549 cell line of human non-small cell lung cancer (NSCLS) And these results do not affect cell proliferative activity and it is confirmed that cancer metastasis and invasion are suppressed in various human cancer cell lines such as breast cancer, colon cancer and prostate cancer as the above results. In addition, EMT inhibitory effect was confirmed in various conditioned media with macrophages, and it was confirmed that the above mechanism works independently of Smad. In addition, PPARγ-dependent PTEN expression was secreted into exosomes in the macrophages stimulated by the killed cancer cells. Secreted PTEN was introduced into 344SQ cancer epithelial cells to maintain cell polarity, anti-EMT, Cancer cell migration and invasion inhibition mechanism. Furthermore, it was confirmed that 15-HETE, lipoxin A4 and 15d-PGJ 2 secretion were increased in the macrophages stimulated by the killed cancer cells. Inhibition of TGF-β1-induced PPPARγ expression and activity and PTEN expression And the reversal effect of conditioned media on inhibition and EMT action was reduced. When these ligands were directly treated with 344SQ cancer cells, expression and activation of TGF-β1-induced PPPARγ and inhibition of PTEN expression were restored, and it was confirmed that EMT was inhibited. In addition, an increase in the expression of PPARy and PTEN in primary tumor tissues and tumor-infiltrating macrophages was confirmed in a mouse animal model, and by confirming the effect of inhibiting tumor metastasis, the conditioned medium of the present invention is the basis of cancer metastasis EMT, migration, stem cell transformati
