TP53INP1高表達(dá)在砷劑殺傷肺腺癌細(xì)胞中的增敏作用
發(fā)布時間:2019-06-18 12:31
【摘要】:目的構(gòu)建TP53INP1高表達(dá)的肺腺癌A549細(xì)胞,初步研究提高TP53INP1的表達(dá)能否提高砷劑對肺腺癌細(xì)胞的殺傷作用。方法構(gòu)建TP53INP1重組真核表達(dá)質(zhì)粒,以慢病毒為載體將其轉(zhuǎn)染到A549細(xì)胞,建立穩(wěn)定高表達(dá)TP53INP1基因的A549-TP53INP1細(xì)胞株,以流式細(xì)胞術(shù)和MTT實驗檢測As_2O_3處理后A549-TP53INP1細(xì)胞的凋亡和存活率。結(jié)果成功構(gòu)建穩(wěn)定A549-TP53INP1細(xì)胞株。流式細(xì)胞術(shù)結(jié)果顯示,相同劑量As2O3作用下(5~40μmol/L),A549-TP53INP1細(xì)胞凋亡率[(15.6±3.5)%]顯著高于A549細(xì)胞[(10.0±2.5)%](P0.05)。MTT實驗顯示,As_2O_3處理后A549-TP53INP1細(xì)胞的IC50值[(44.64±6.84)μmol/L]顯著低于A549細(xì)胞[(54.25±6.13)μmol/L](P0.05)。結(jié)論 TP53INP1高表達(dá)可增加砷劑對肺腺癌細(xì)胞的殺滅作用,提示TP53INP1可作為砷劑治療肺癌的增敏靶點。
[Abstract]:Objective to construct lung cancer cell line A549 with high expression of TP53INP1 and to study whether increasing the expression of TP53INP1 can increase the killing effect of arsenic on lung adenocarcinoma cell line. Methods the recombinant eukaryotic expression plasmid TP53INP1 was constructed and transformed into A549 cells with lentivirus as vector. The A549-TP53INP1 cell line with stable and high expression of TP53INP1 gene was established. The apoptosis and survival rate of A549-TP53INP1 cells treated with As_2O_3 were detected by flow cytometry and MTT assay. Results stable A549-TP53INP1 cell line was successfully constructed. The results of flow cytometry showed that the apoptosis rate of (5 ~ 40 渭 mol / L), A549-TP53INP1) cells [(15.6 鹵3.5)%] was significantly higher than that of A549 cells [(10.0 鹵2.5)%] (P 0.05). The IC50 value of A549-TP53INP1 cells treated with As_2O_3 [(44.64 鹵6.84) 渭 mol/L] was significantly lower than that of A549 cells [(54.25 鹵6.13) 渭 mol/L] (P 0.05). Conclusion the high expression of TP53INP1 can increase the killing effect of arsenic on lung cancer cells, suggesting that TP53INP1 can be used as a sensitizing target for arsenic in the treatment of lung cancer.
【作者單位】: 四川大學(xué)華西公共衛(wèi)生學(xué)院環(huán)境衛(wèi)生與職業(yè)醫(yī)學(xué)系;
【基金】:國家自然科學(xué)基金面上項目(No.81372945)
【分類號】:R734.2
[Abstract]:Objective to construct lung cancer cell line A549 with high expression of TP53INP1 and to study whether increasing the expression of TP53INP1 can increase the killing effect of arsenic on lung adenocarcinoma cell line. Methods the recombinant eukaryotic expression plasmid TP53INP1 was constructed and transformed into A549 cells with lentivirus as vector. The A549-TP53INP1 cell line with stable and high expression of TP53INP1 gene was established. The apoptosis and survival rate of A549-TP53INP1 cells treated with As_2O_3 were detected by flow cytometry and MTT assay. Results stable A549-TP53INP1 cell line was successfully constructed. The results of flow cytometry showed that the apoptosis rate of (5 ~ 40 渭 mol / L), A549-TP53INP1) cells [(15.6 鹵3.5)%] was significantly higher than that of A549 cells [(10.0 鹵2.5)%] (P 0.05). The IC50 value of A549-TP53INP1 cells treated with As_2O_3 [(44.64 鹵6.84) 渭 mol/L] was significantly lower than that of A549 cells [(54.25 鹵6.13) 渭 mol/L] (P 0.05). Conclusion the high expression of TP53INP1 can increase the killing effect of arsenic on lung cancer cells, suggesting that TP53INP1 can be used as a sensitizing target for arsenic in the treatment of lung cancer.
【作者單位】: 四川大學(xué)華西公共衛(wèi)生學(xué)院環(huán)境衛(wèi)生與職業(yè)醫(yī)學(xué)系;
【基金】:國家自然科學(xué)基金面上項目(No.81372945)
【分類號】:R734.2
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