Abstract
Background: Sorafenib is a multi-target kinase inhibitor that has been approved as a unique target drug for the treatment of advanced hepatocellular carcinoma (HCC). However, due to the frequent occurrence of drug resistance, its treatment efficacy is often limited. The aim of this study was to explore the function of HOX transcript antisense intergenic RNA (HOTAIR) for the treatment of HCC with sorafenib, and its underlying mechanism. Methods: A cell counting kit-8 (CCK-8) assay and Edu assay were used to examine the viability and proliferation of HCC cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of HOTAIR and miR-217 in HCC cells. Small interfering (si) RNA was transfected to knockdown HOTAIR to explore its biological function. A Western blot and immunofluorescence were performed to detect the level of E-cadherin and Vimentin expression. Results: Sorafenib resistance was increased in HCC cells with high HOTAIR expression. Moreover, a knockdown of HOTAIR could improve the therapeutic effect of sorafenib on HCC via increasing E-cadherin and decreasing Vimentin expression. Additionally, a HOTAIR knockdown could increase the sensitivity of sorafenib for HCC treatment by up-regulating miR-217. Conclusions: Lnc HOTAIR could increase sorafenib resistance in HCC by inhibiting miR-217. Our research attempts to elucidate a more effective treatment and provides novel insight into potential clinical treatment for HCC.