목적: Overexpression of long non-coding RNA HOTAIR has been reported in several types of cancer. Although HOTAIR has been associated with metastasis and poor prognosis in different tumor types, a deep characterization of its fuctions in cancer is still needed. The epithelial to mesemchymal transition (EMT) promotes cervical cancer progression, and HOTAIR have been found to be act as a key regulator of EMT. The aim of the present study was to investigate the functional roles of HOTAIR in EMT and cervical cancer progression. 방법: Serum levels of HOTAIR were assessed in 123 cervical cancer patients and 20 normal volunteers by real-time RT-PCR. Proliferation, invasion, and wound healing assays were used to investigate the biological role of HOTAIR in cervical cancer cells, by exposure of HeLa and SiHa cells to HOTAIR. 결과: The serum levels of HOTAIR in cervical cancer patients were significantly higher than that in normal volunteers. HOTAIR knockdown (siHOTAIR) inhibited cell proliferation, migration. In addition, inhibition of HOTIAR in cervical cancer cells could reduce invasiveness, as well as the expression of MMP-2 and MMP-9. Knockdown of HOTAIR decreased the EMT characterized by impared N-cadherin, β-catenin, and vimentin and induction of E-cadherin in vitro. Furthermore, siHOTAIR downregulated the expression of EMP transcription factors Snail and Twist. 결론: These results suggest that HOTAIR may play an important role in the progression of cervical cancer through the induction of EMT.