Original Article
Knockdown of HOTAIR reduces the malignancy of bladder cancer cells via downregulation of invasions and metastasis-related genes
Abstract
Background: Bladder cancer is one of the most common malignant tumors. However, the mechanisms underlying the malignancy of the cancer remain largely unknown. This study was conducted to explore the effect of silencing long non-coding RNA (LncRNA) HOX transcript antisense intergenic RNA (HOTAIR) on the biological features of bladder cancer.
Methods: The HOTAIR gene in human bladder cancer cell line 253J was knockdown with siHOTAIR. Cell proliferation and apoptosis were determined using the CCK8 and Hoechst assays, respectively. The expression of Notch1, EpCAM, CXCR2, E-cadherin, vimentin, MMP-2 and α-SMA was measured using qPCR and Western blot analysis.
Results: Compared with the controls, the expression of HOTAIR decreased significantly after the cells were transfected with siHOTAIR, indicating that HOTAIR was down-regulated. After the cells were transfected with siHOTAIR, the OD value was significantly decreased, cell apoptosis was significantly increased, the expression of Notch1, EpCAM, CXCR2, vimentin, MMP-2 and α-SMA was decreased significantly, while the expression of E-cadherin was significantly increased (P<0.05). More cells were observed in S stage than in G stage following the siHOTAIR transfection.
Conclusions: siHOTAIR reduces the expression of HOTAIR and inhibits the proliferation of bladder cancer cells. These data further our understanding of the metastasis of bladder cancer and provide new clues for the diagnosis and treatment of bladder cancer.
Methods: The HOTAIR gene in human bladder cancer cell line 253J was knockdown with siHOTAIR. Cell proliferation and apoptosis were determined using the CCK8 and Hoechst assays, respectively. The expression of Notch1, EpCAM, CXCR2, E-cadherin, vimentin, MMP-2 and α-SMA was measured using qPCR and Western blot analysis.
Results: Compared with the controls, the expression of HOTAIR decreased significantly after the cells were transfected with siHOTAIR, indicating that HOTAIR was down-regulated. After the cells were transfected with siHOTAIR, the OD value was significantly decreased, cell apoptosis was significantly increased, the expression of Notch1, EpCAM, CXCR2, vimentin, MMP-2 and α-SMA was decreased significantly, while the expression of E-cadherin was significantly increased (P<0.05). More cells were observed in S stage than in G stage following the siHOTAIR transfection.
Conclusions: siHOTAIR reduces the expression of HOTAIR and inhibits the proliferation of bladder cancer cells. These data further our understanding of the metastasis of bladder cancer and provide new clues for the diagnosis and treatment of bladder cancer.
