CAJ | 학술논문

目的：探讨钙黏蛋白表达与表皮生长因子受体( EGFR)分子靶向治疗敏感或耐药的相关性。方法乳腺癌细胞(MCF-7和MDA-MB-231)、膀胱癌细胞株(T24)、子宫颈鳞癌细胞(SiHa)、大细胞肺癌细胞株(H460)、肝癌细胞株( SK-HEP-1和MHCC97-H)以及单核细胞白血病( THP-1)等8种细胞分别用表皮生长因子受体酪胺酸激酶抑制药(EGFR-TKI)PD153035和吉非替尼处理48 h,采用噻唑蓝(MTT)法检测其敏感或耐药性,计算各细胞的半数抑制浓度(IC50),并与各细胞钙黏蛋白水平比较,观察相关性。结果随着PD153035和吉非替尼浓度的升高,MCF-7、MDA-MB-231、T24及SiHa细胞生存率明显下降,表现为敏感,钙黏蛋白表达阳性； H460、SK-HEP-1、MHCC97-H及THP-1细胞生存率未见明显下降,表现为耐药,钙黏蛋白表达阴性。结论EGFR-TKI对上皮性肿瘤细胞的生存率与钙黏蛋白的表达水平存在相关性；钙黏蛋白可能在调节EGFR分子靶向治疗的敏感性方面起重要作用；钙黏蛋白作为标志物为临床筛选合适的患者进行EGFR-TKI分子靶向治疗提供了重要线索。
목적：탐토개점단백표체여표피생장인자수체( EGFR)분자파향치료민감혹내약적상관성。방법유선암세포(MCF-7화MDA-MB-231)、방광암세포주(T24)、자궁경린암세포(SiHa)、대세포폐암세포주(H460)、간암세포주( SK-HEP-1화MHCC97-H)이급단핵세포백혈병( THP-1)등8충세포분별용표피생장인자수체락알산격매억제약(EGFR-TKI)PD153035화길비체니처리48 h,채용새서람(MTT)법검측기민감혹내약성,계산각세포적반수억제농도(IC50),병여각세포개점단백수평비교,관찰상관성。결과수착PD153035화길비체니농도적승고,MCF-7、MDA-MB-231、T24급SiHa세포생존솔명현하강,표현위민감,개점단백표체양성； H460、SK-HEP-1、MHCC97-H급THP-1세포생존솔미견명현하강,표현위내약,개점단백표체음성。결론EGFR-TKI대상피성종류세포적생존솔여개점단백적표체수평존재상관성；개점단백가능재조절EGFR분자파향치료적민감성방면기중요작용；개점단백작위표지물위림상사선합괄적환자진행EGFR-TKI분자파향치료제공료중요선색。
Objective To explore the correlation of E-cadherin expression and the sensitivity to EGFR-TKI molecular targeted therapy. Methods Eight kinds of cells,MCF-7,MDA-MB-231,T24,SiHa,H460,SK-HEP-1,MHCC97-H and THP-1 were treated with EGFR-TKI PD153035 and gefitinib,respectively,for 48 hours. The drug-sensitivity was detected by MTT,and the IC50 of cells were calculated. The E-cadherin protein were detected and compared. Results Followed with PD153035 and gefitinib treatment,the survival rates of MCF-7,MDA-MB-231,T24 and SiHa significantly reduced,and more E-cadherin protein expressed. However, the survival rates of the H460, SK-HEP-1, MHCC97-H, and THP-1 cells showed opposite results. Conclusion The sensitivity of epithelial cancer cells to EGFR-TKI is correlated with E-cadherin expression. E-cadherin may play a significant role on regulateing the sensitivity to EGFR-TKI molecular targeted therapy. E-cadherin is a key biomarker for recruiting appropriate patients for EGFR-TKI molecular targeted therapy.