中国临床药理学杂志2018，Vol.34Issue(19)：2320-2323,4.DOI:10.13699/j.cnki.1001-6821.2018.19.022
长链非编码RNA RMRP通过JAK2/STAT3信号通路增强胶质瘤细胞对替莫唑胺敏感性的机制研究
Mechanisms of long noncoding RNA RMRP enhanced glioma cell chemo-sensitivity to temozolomide through JAK2 /STAT3 signaling pathway
摘要
Abstract
Objective To investigate the effect of long noncoding RNA RMRP( lncRNA -RMRP) on the temozolomide ( TMZ ) resistance of glioma cells and to detect the expression of lncRNA -RMRP in regular glioma cells (U87, U118) and TMZ-resistant glioma cells ( U87TR, U118TR), primary glioma tissues and relapsed glioma tissues .Methods Real-time quantita-tive PCR was used to detect the expression of lncRNA -RMRP in cell lines (U87, U118, U87TR, U118TR), primary and relapsed glioma tissues.U87TR and U118TR cells were transfected with lncRNA -RMRP.The experiment was di-vided into four groups: U87TR-RMRP, U87TR-NC, U118TR-RMRP and U118TR-NC.The viability of U87, U118, U87TR and U118TR cells was tested by CCK -8 assay at 0, 24, 48, 72 and 96 hours after TMZ (400 μmol· L-1) treatment.50%inhibiting concentration ( IC50) was used to evaluate the resistance to TMZ in each treat-ment group.The expression of JAK2/STAT3 protein in each group was detected by Western blot .Results Real-time quantitative PCR showed that the expressions of LncRNA -RMRP were U87 ( 1.03 ±0.21 ) vs. U87TR (0.12 ±0.07), U118 (1.07 ±0.32) vs.U118TR (0.43 ±0.15), relapsed glioma tissues (1.36 ±0.78) vs.prima-ry glioma tissues ( 3.41 ±1.61 ), and the difference were statistically significant ( all P <0.01 ) .The results of CCK-8 assay showed that the proliferative ability of U87 and U87TR were (2.62 ±0.22) and (4.01 ±0.12), U118 and U118TR were (2.45 ±0.09) and (4.47 ±0.09), the differences were statistically significant (all P<0.01). IC50of U87 and U87TR were (99.33 ±9.02 ) and (253.30 ±15.28 ) μmol· L-1, which in U118 and U118TR were (100.00 ±10.00 ) and (233.30 ±15.28 ) μmol· L-1, the differences were statistically significant ( all P<0.01 ). The results of CCK -8 assay showed that the proliferative ability of U 87TR -RMRP and U87TR -NC were (2.18 ±0.14) and (4.36 ±0.13), U118TR-RMRP and U118TR-NC were (3.25 ±0.21) and (4.29 ±0.11), the differences were statistically significant (all P<0.01).IC50of U87TR-RMRP and U87TR-NC groups were (142.30 ±6.81) and (283.30 ±15.28)μmol· L-1, which in U118TR -RMRP and U118TR-NC groups were (189.70 ±16.01) and (300.30 ±10.02)μmol· L-1, the differences were statistically significant (all P<0.01).In U87TR-RMRP and U87TR -NC groups, p -JAK2 were (1.02 ±0.23 ) and (0.49 ±0.13 ), p -STAT3 were (1.02 ±0.0.21 ) and (0.28 ±0.07 ), the differences were statistically significant ( all P <0.05 ) .In U118TR -RMRP and U87TR-NC groups, p-JAK2 were (1.00 ±0.13) and (0.29 ±0.04), p-STAT3 were (1.09 ±0.27) and (0.36 ±0.04), the differences were statistically significant (all P<0.01).Conclusion LncRNA-RMRP can enhance the sensitivity of glioma cells to TMZ through JAK 2/STAT3 signaling pathway.关键词
替莫唑胺/长链非编码RNA RMRP/胶质瘤/耐药性Key words
temozolomide/long noncoding RNA RMRP/glioma/chemo-resistance分类
医药卫生引用本文复制引用
马飞,李令兴,李琳,姜志平,高培平..长链非编码RNA RMRP通过JAK2/STAT3信号通路增强胶质瘤细胞对替莫唑胺敏感性的机制研究[J].中国临床药理学杂志,2018,34(19):2320-2323,4.基金项目
中国医药教育协会基金资助项目(2016SKT-M030) （2016SKT-M030）
