In summary, our findings suggest that upregulated BTG1 expression might suppress the aggressive phenotypes of ovarian carcinoma cells by downregulating expression of the phenotype-related genes and subsequently their encoded protein products, such as members of the PI3K-Akt pathway, Bcl-xL, survivin; VEGF; and MMP-2 which promote proliferation, anti-apoptosis, and invasion, respectively [27–29]. Here, BCL2L1 is linked to ovarian carcinoma.