中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2012年
5期
805-808
,共4页
王汉晋%林彩玲%蔡永东%翟长元
王漢晉%林綵玲%蔡永東%翟長元
왕한진%림채령%채영동%적장원
表皮生长因子受体%丝氨酸/苏氨酸蛋白激酶%三苯氧胺%耐药%乳腺癌
錶皮生長因子受體%絲氨痠/囌氨痠蛋白激酶%三苯氧胺%耐藥%乳腺癌
표피생장인자수체%사안산/소안산단백격매%삼분양알%내약%유선암
Epidermal growth factor receptor%Protein kinase B%Tamoxifen%Drug resistance%Breast carcinoma
目的 观察表皮生长因子受体( EGFR)/丝氨酸/苏氨酸蛋白激酶(AKT)途径在三苯氧胺(TAM)耐药人乳腺癌细胞株MCF-7形成过程的变化,及抑制该途径对肿瘤细胞周期的影响.方法 用1×10-7 nmoL/L的三苯氧胺诱导、建立三苯氧胺耐药细胞(TAM-R)细胞株,以荧光定量逆转录聚合酶链反应( fqRT-PCR)、Western blot法、流式细胞术检测MCF-7与TAM-R细胞中EGFR mRNA、p-AKT蛋白的表达及TAM-R细胞给予EGFR及AKT抑制剂后对细胞周期的影响.结果 TAM-R细胞中EGFR mRNA和p-AKT蛋白的表达较MCF-7显著提高(P＜0.05)；给予ZD1839和SH-6阻断EGFR/AKT信号通路后,p-AKT表达受到抑制(P＜0.05),TAM-R细胞的G0～G1期比例提高,其中20 μmol/L ZD1839组高达88％,细胞增殖指数下降(P＜0.05).结论 EGFR/AKT信号通路在MCF-7细胞对TAM耐药的形成中提供了非雌激素途径的生长信号.
目的 觀察錶皮生長因子受體( EGFR)/絲氨痠/囌氨痠蛋白激酶(AKT)途徑在三苯氧胺(TAM)耐藥人乳腺癌細胞株MCF-7形成過程的變化,及抑製該途徑對腫瘤細胞週期的影響.方法 用1×10-7 nmoL/L的三苯氧胺誘導、建立三苯氧胺耐藥細胞(TAM-R)細胞株,以熒光定量逆轉錄聚閤酶鏈反應( fqRT-PCR)、Western blot法、流式細胞術檢測MCF-7與TAM-R細胞中EGFR mRNA、p-AKT蛋白的錶達及TAM-R細胞給予EGFR及AKT抑製劑後對細胞週期的影響.結果 TAM-R細胞中EGFR mRNA和p-AKT蛋白的錶達較MCF-7顯著提高(P＜0.05)；給予ZD1839和SH-6阻斷EGFR/AKT信號通路後,p-AKT錶達受到抑製(P＜0.05),TAM-R細胞的G0～G1期比例提高,其中20 μmol/L ZD1839組高達88％,細胞增殖指數下降(P＜0.05).結論 EGFR/AKT信號通路在MCF-7細胞對TAM耐藥的形成中提供瞭非雌激素途徑的生長信號.
목적 관찰표피생장인자수체( EGFR)/사안산/소안산단백격매(AKT)도경재삼분양알(TAM)내약인유선암세포주MCF-7형성과정적변화,급억제해도경대종류세포주기적영향.방법 용1×10-7 nmoL/L적삼분양알유도、건립삼분양알내약세포(TAM-R)세포주,이형광정량역전록취합매련반응( fqRT-PCR)、Western blot법、류식세포술검측MCF-7여TAM-R세포중EGFR mRNA、p-AKT단백적표체급TAM-R세포급여EGFR급AKT억제제후대세포주기적영향.결과 TAM-R세포중EGFR mRNA화p-AKT단백적표체교MCF-7현저제고(P＜0.05)；급여ZD1839화SH-6조단EGFR/AKT신호통로후,p-AKT표체수도억제(P＜0.05),TAM-R세포적G0～G1기비례제고,기중20 μmol/L ZD1839조고체88％,세포증식지수하강(P＜0.05).결론 EGFR/AKT신호통로재MCF-7세포대TAM내약적형성중제공료비자격소도경적생장신호.
Objective To investigate the change of epidermal growth factor receptor/protein kinase B (EGFR/AKT) signaling pathway in the generation of tamoxifen (TAM) resistant MCF-7 breast cancer cells and the impact on the tumor cell cycle by suppressing EGFR/AKT signaling pathway.Methods The TAM-R was derived from the wild type MCF-7 breast cancer cells continuously exposed to 1 × 10-7 nmol/L 4-hydroxy tamoxifen for 6 months. EGFR mRNA and p-AKT were detected by using fluorescent quantitation reverse transcription-polymerase chain reaction (fqRT-PCR) and Western blotting,respectively.Cell cycle was tested by flow cytometry.Results The expression levels of EGFR mRNA and p-AKT protein in TAM-R cells were higher (P＜0.05) than those in MCF-7 cells.lnhibitors,ZD1839 and SH-6,suppressed the expression of p-AKT and the proliferation of TAM-R cells significantly.Conclusion The activation of EGFR/AKT signaling pathway may provide other growth signal,not estrogen,in tamoxifen resistant MCF-7 cells.
