Xia Wang1,2, Wei Liu3, Peiyuan Wang3, Shu Li1. 1. Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Department of Periodontology, School of Stomatology, Shandong University, Jinan, Shandong, China. 2. Department of Oral Pathology, Binzhou Medical University, Yantai, Shandong, China. 3. Medical Imaging Research Institute, Binzhou Medical University, Yantai, Shandong, China.
Abstract
BACKGROUND: Long noncoding RNA HOX transcript antisense RNA (lncRNA HOTAIR) is overexpressed in many types of human cancers and is correlated with clinical stage and lymph node metastasis in oral squamous cell carcinoma (OSCC). Autophagy, an important mechanism of self-protection, plays vital roles in adapting to hypoxia, tolerating external stimulation, and inducing chemotherapy resistance in OSCC cells. This study aims to investigate the effect of HOTAIR on autophagy, apoptosis, and invasion of OSCC cells. METHODS: HOTAIR expression in OSCC cells was knocked down by small RNA interference. Transmission electron microscope, Western blot, and flow cytometry assay were used to detect the level of autophagy and apoptosis. OSCC cells were medicated with cisplatin, and median lethal dose (LD50) was performed to evaluate the effect on chemosensitivity of HOTAIR. RESULTS: After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. Proliferation, migration, and invasion of OSCC cells were suppressed. Furthermore, apoptosis rate was enhanced, and the sensitivity to cisplatin was promoted when compared with the negative control group. CONCLUSION: HOTAIR acts as an oncogene in OSCC cells, and HOTAIR silence may be a potential therapeutic target for OSCC.
BACKGROUND: Long noncoding RNA HOX transcript antisense RNA (lncRNA HOTAIR) is overexpressed in many types of humancancers and is correlated with clinical stage and lymph node metastasis in oral squamous cell carcinoma (OSCC). Autophagy, an important mechanism of self-protection, plays vital roles in adapting to hypoxia, tolerating external stimulation, and inducing chemotherapy resistance in OSCC cells. This study aims to investigate the effect of HOTAIR on autophagy, apoptosis, and invasion of OSCC cells. METHODS:HOTAIR expression in OSCC cells was knocked down by small RNA interference. Transmission electron microscope, Western blot, and flow cytometry assay were used to detect the level of autophagy and apoptosis. OSCC cells were medicated with cisplatin, and median lethal dose (LD50) was performed to evaluate the effect on chemosensitivity of HOTAIR. RESULTS: After HOTAIR silence, autophagy was inhibited with the downregulated expression of MAP1LC3B (microtubule-associated protein 1 light chain 3B), beclin1, and autophagy-related gene (ATG) 3 and ATG7. The expressions of mTOR increased. Proliferation, migration, and invasion of OSCC cells were suppressed. Furthermore, apoptosis rate was enhanced, and the sensitivity to cisplatin was promoted when compared with the negative control group. CONCLUSION:HOTAIR acts as an oncogene in OSCC cells, and HOTAIR silence may be a potential therapeutic target for OSCC.