Tiejun Song1,1, Lei Yan2,1, Kerui Cai2, Tianshu Zhao3, Meiling Xu4. 1. Department of Clinical Laboratory, The Second Affiliated Hospital of Mudanjiang Medical University, Mudanjiang 157011, Heilongjiang, China. 2. Department of Histology and Embryology, Mudanjiang Medical University, Mudanjiang 157011, Heilongjiang, China. 3. Department of Neurosurgery, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China. 4. Department of Neurology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China.
Abstract
BACKGROUND: Drug resistance in clinical cancer treatment has become an issue. OBJECTIVE: We focus on abnormally expressed lncRNAs in glioma and investigating the function of PVT1. METHODS: The paclitaxel-resistant glioma cells SHG-44 RE was obtained through screening the SHG 44 cells that were cultured in medium containing a certain concentration of paclitaxel. Cell survival of SHG 44 RE and SHG 44 cells under the treatment of paclitaxel was detected by MTT assay. The aberrant expressed lncRNAs were screened out with microarray analysis. Further qRT-PCR was utilized to validate the expression of lncRNA PVT1 in the two cells. After manipulating the expression of PVT1, cell viability and apoptosis were measured by MTT and flow cytometry respectively. RESULTS: LncRNA PVT1 was overexpressed in glioma cells SHG-44 RE compared with parent SHG-44 cells. Down-regulation of lncRNA PVT1 inhibited the SHG-44 RE cell viability and increased glioma SHG-44 RE cells apoptosis after paclitaxel treatment, suggesting that inhibition of lncRNA PVT1 improved paclitaxel sensibility in human glioma cells. CONCLUSION: Down-regulation of PVT1 could enhance chemosensitivity of paclitaxel, induce apoptosis of glioma cells and noteworthy inhibit glioma cells proliferation. Our findings of PVT1 could contribute to attenuate paclitaxel resistance in clinical medicine.
BACKGROUND: Drug resistance in clinical cancer treatment has become an issue. OBJECTIVE: We focus on abnormally expressed lncRNAs in glioma and investigating the function of PVT1. METHODS: The paclitaxel-resistant glioma cells SHG-44 RE was obtained through screening the SHG 44 cells that were cultured in medium containing a certain concentration of paclitaxel. Cell survival of SHG 44 RE and SHG 44 cells under the treatment of paclitaxel was detected by MTT assay. The aberrant expressed lncRNAs were screened out with microarray analysis. Further qRT-PCR was utilized to validate the expression of lncRNA PVT1 in the two cells. After manipulating the expression of PVT1, cell viability and apoptosis were measured by MTT and flow cytometry respectively. RESULTS: LncRNA PVT1 was overexpressed in glioma cells SHG-44 RE compared with parent SHG-44 cells. Down-regulation of lncRNA PVT1 inhibited the SHG-44 RE cell viability and increased glioma SHG-44 RE cells apoptosis after paclitaxel treatment, suggesting that inhibition of lncRNA PVT1 improved paclitaxel sensibility in humanglioma cells. CONCLUSION: Down-regulation of PVT1 could enhance chemosensitivity of paclitaxel, induce apoptosis of glioma cells and noteworthy inhibit glioma cells proliferation. Our findings of PVT1 could contribute to attenuate paclitaxel resistance in clinical medicine.