Luo Qingying, Gu Shiyan, Li Yang, Zhang Zunzhen
Department of Environmental Health, West China School of Public Health, Sichuan University, Chengdu 610041, China.
Wei Sheng Yan Jiu. 2017 Jan;46(1):120-125.
To explore if improving the expression of TP53INP1 could enhance the sensitivity of A549 cells to arsenic.
The eukaryotic express vector containing TP53INP1 gene was transferred into A549 cells by using lentivirus vector. Cell apoptosis and cell viability after arsenic treatment were assessed by flow cytometry and MTT assay, respectively.
The protein expression level of TP53INP1 was increased in A549 cells transferred with eukaryotic express vector containing TP53INP1 gene, which led to an increase in apoptosis and a decrease in cell viability. Compared with A549 cells, significant increase in apoptosis was found in A549-TP53INP1 cells when treated with As_2O_3( 5- 40 μmol/L). In addiation, the IC50 of As_2O_3 in A549-TP53INP1(( 44. 64 ± 6. 84) μmol/L) cells was significantly lower than that of the A549 group(( 54. 25 ± 6. 13) μmol/L)( P < 0. 05).
Enhancement of TP53INP1 can significantly improve apoptosis response and enhance sensitivity of A549 cells to arsenic. It is suggested that TP53INP1 could be used as a new target in arsenic-based cancer treatment.
探讨提高TP53INP1的表达是否能增强A549细胞对砷的敏感性。
利用慢病毒载体将含TP53INP1基因的真核表达载体转入A549细胞。分别采用流式细胞术和MTT法评估砷处理后的细胞凋亡和细胞活力。
转染含TP53INP1基因真核表达载体的A549细胞中TP53INP1蛋白表达水平升高，导致细胞凋亡增加，细胞活力降低。与A549细胞相比，用As₂O₃（5 - 40 μmol/L）处理时，A549 - TP53INP1细胞凋亡显著增加。此外，A549 - TP53INP1细胞中As₂O₃的IC50（（44.64 ± 6.84）μmol/L）显著低于A549组（（54.25 ± 6.13）μmol/L）（P < 0.05）。
增强TP53INP1可显著改善凋亡反应，增强A549细胞对砷的敏感性。提示TP53INP1可作为砷基癌症治疗的新靶点。
