Objectives: Interleukin-17 (IL-17) induced chronic inflammation has been associated with development, invasion, and metastasis of tumors, which has been demonstrated to promote development of ovarian cancer, prostate cancer, colon cancer, skin cancer, breast cancer, lung cancer and pancreatic cancer. The present authors found that IL-17 promoted ovarian cancer developed, in addition, with a concurrent increase of metastasis-associated genes-1 (MTA1). Whether IL-17 mediates MTA1’s action and the underlying mechanisms remain unknown. Material and Methods: Cell invasion was detected by wound-healing assay and transwell assay after treatment with IL-17 at 20 ng/ml concentrations for 24 hours. The apoptotic rates of cells were detected by a flow cytometer (FCM) after IL-17 treatment at 20 ng/ml concentrations for 24 hours. The expression of MTA1, Vimentin, Twist, Snail, Slug, N-cadherin, and E-cadherin was detected by Western blot analysis and reverse transcription polymerase chain reaction (RT-PCR) after treatment with 20 ng/ml of IL- 17 for 8, 16, 24, and 36 hours, respectively. Results: Wound-healing assay and transwell assay demonstrated IL-17 increases ovarian carcinoma cell invasion, and the FCM showed that the apoptotic rates in the IL-17 group were lower than those in the control group (p < 0.01). Western blot analysis detected that MTA1, Vimentin, Twist, Snail, slug, and N-cadherin in the IL-17 group were higher than those in the control group, E-cadherin in the IL-17 group were lower than those in the control group, and RT-PCR detected that MTA1 mRNA levels were positively correlated with the time of IL-17 affected on ovarian carcinoma cells (p < 0.05). Conclusions: IL-17 induces MTA1 expression to enhancing epithelial-to-mesenchymal transition (EMT) and tumor cell invasion, which indicates IL-17- MTA1-EMT axis as potential targets for developing new strategies in the prevention and treatment of ovarian cancer.