CAJ | 학술논문

目的：探索活化型信号转导子和转录激活子3蛋白抑制剂(PIAS3)对肺腺癌A549细胞增殖的影响及相关意义，为进一步研究利用辐射应答基因启动子驱动的PIAS3腺相关病毒载体联合放射治疗肺腺癌提供基础。方法：利用MTT比色试验和克隆形成率实验检测转染pCMV-Sport6-PIAS3后对肺腺癌细胞A549存活和增殖的影响；利用免疫荧光染色实验检测共转染pCMV-Sport6-PIAS3、PRC-CMV、PRC-STAT3及PRC-STAT3-CT后对p-STAT3入核的影响。结果：PIAS3过表达导致A549细胞生长显著抑制，克隆形成能力显著降低；免疫荧光染色实验结果表明，转染pCMV-Sport6-PIAS3后，STAT3入核被显著抑制，通过共转染表达STAT3和STAT3-CT后，STAT3入核仍显著受到抑制。结论：PIAS3过表达可抑制STAT3的入核，继而阻断其功能，从而降低肺腺癌细胞A549的生长和增殖能力。
목적：탐색활화형신호전도자화전록격활자3단백억제제(PIAS3)대폐선암A549세포증식적영향급상관의의，위진일보연구이용복사응답기인계동자구동적PIAS3선상관병독재체연합방사치료폐선암제공기출。방법：이용MTT비색시험화극륭형성솔실험검측전염pCMV-Sport6-PIAS3후대폐선암세포A549존활화증식적영향；이용면역형광염색실험검측공전염pCMV-Sport6-PIAS3、PRC-CMV、PRC-STAT3급PRC-STAT3-CT후대p-STAT3입핵적영향。결과：PIAS3과표체도치A549세포생장현저억제，극륭형성능력현저강저；면역형광염색실험결과표명，전염pCMV-Sport6-PIAS3후，STAT3입핵피현저억제，통과공전염표체STAT3화STAT3-CT후，STAT3입핵잉현저수도억제。결론：PIAS3과표체가억제STAT3적입핵，계이조단기공능，종이강저폐선암세포A549적생장화증식능력。
Objective: To explore the effect of PIAS3 on proliferation of lung adenocarcinoma A549 cells, in order to provide a foundation for the further study in which a adeno-associated virus (AAV) containing PIAS3 gene driven by a radiation response promoter plus radiotherapy will be used to treatment lung adenocarcinoma. Methods: The growth and proliferation of A549 cells transfected with pCMV-Sport6-PIAS3 plasmid were detected by MTT assay and cloning forming efficiency assay. The nucleus translocation of p-STAT3 was detected by immunofluorescence staining after CMV-Sport6-PIAS3 was co-transfected with PRC-CMV, PRC-STAT3 or PRC-STAT3-CT. Results:The growth and cloning form of A549 cells were significantly inhibited by PIAS3 overexpression. The result of immunofluorescence staining indicated that the nucleus translocation of p-STAT3 as significantly blocked by transfection with pCMV-Sport6-PIAS3, even after co-transfection with STAT3 or STAT3-CT. Conclusion: The overexpression of PIAS3 could inhibit the nucleus translocation of STAT3, which subsequently blocked the function of STAT3 and decreased the ability of growth and proliferation of A549 cells.