Study on augementation of chemotherapeutic effect by anticancer drugs in human lung cancers: Analysis of drug resistance in cancer cells.

肿瘤治疗过程中抗癌药物的无效是由于肿瘤细胞自身的耐药机制所致，本文以耐药蛋白金属硫蛋白(MT)为研究对象，通过培养的人肺腺癌细胞对其耐药机制进行了分析。用顺铂(Cys)处理癌细胞。用相差显微镜、扫描电子显微镜、荧光显微镜和流式细胞仪对半胱氨酸作用下的活细胞进行观察。细胞提取液和培养上清液中的MT用Sephadex G-75柱洗脱，将细胞分为死亡细胞和静息细胞(RC)。在添加EGF、纤维连接蛋白和胰岛素作为生长因子的情况下，RC重新生长，并由不同的细胞群组成。其中一种尺寸较大，另一种工艺较长。FVM显示，Rc明显大于原始细胞(OC)，且内、表面结构不同。扫描电子显微镜显示RC的微血管变短，OC的小泡样突起消失。倍增时间：RC为48h，INOC为71h。免疫荧光实验显示RC提取液和培养上清液中的细胞标志物CEA降低，角蛋白升高，而HLA值无明显变化，Sephadex G-75图谱显示RC提取液和培养上清液中均含有MT。

It is known that non efficacy of anti cancer drugs during treatment of the malignancy is due to the resistant mechanism in cancer cell itselves, is designed to analyze this resistant mechanism focusing upon the resistant protein metallothioneim(MT).The resistant mechanism was analyzed by means of cultured human adenocarcinoma cells of the lung. This cancer cells were treated with cis-platinum(Cys). Aliving cells cultured with Cys were observed by phase contrast microscope, scanning electro microscope (SEM), fluororescence microscope and flow cytemtry(FCM). MT in cell extract and cultured supernate was eluated by Sephadex G-75 column.Tese cells were divided to died cells and rested cells(RC). The RC re-growthed by added EGF, fibronectin and insulin as growth factors and consisted of different kind of cell groups. Nemely one has large size and another has long process. By FVM, the RC were grossly largeer than orignal cells(OC) and have different stracture both in inside and cell surface. SEM showed microviel in RC become shorter and small bleb like process in OC was lost. Doubling time was 48 h in RC and 71 h inOC. As cell marker, CEA was decreased, keratin increased and HLA not change in RC by observation with immunofluorecence tests, Sephadex G-75 profiles showed MT in RC extract and cultured supernate.In conclusion, the resistant mechanism of RC was regulated by the resistant protein,MT.