In this study, we demonstrate that the constitutively activated STAT3 promotes EMT and inhibits the ERS-associated autophagy, leading to ovarian cancer cell proliferation, metastasis, and cisplatin resistance through a crosstalk with p53 and RAS signaling molecules including Slug, MAPK and PI3K/AKT/mTOR. This evidence concerns the gene SNAI2 and ovarian carcinoma.