Frankfurt O S, Sugarbaker E V, Robb J A, Villa L
Department of Pathology, Cedars Medical Center, Miami, FL 33136, USA.
Cancer Lett. 1995 Nov 6;97(2):149-54. doi: 10.1016/0304-3835(95)03970-8.
Breast cancer cells are relatively resistant to the induction of apoptosis (AP) and drug regimens which readily activate apoptotic death, may enhance the antitumor effect. Rapid and intensive induction of apoptosis was observed in estrogen receptor positive and negative breast cancer cell cultures treated with tamoxifen (TMX) combined with the calmodulin antagonists trifluoperazine (TFP) or W7. TMX (1-5 microM) alone or calmodulin antagonists alone did not induce apoptosis. Importantly, intensive apoptosis was also induced by TMX and TFP in the cells obtained from primary human breast carcinomas. Inhibition of the Ca2+ calmodulin signaling pathway is an effective way to activate apoptotic death in epithelial cells. Combination of TMX with non-toxic calmodulin inhibitors may increase the preventive and therapeutic effects of TMX.
乳腺癌细胞对凋亡诱导相对具有抗性,而那些能轻易激活凋亡性死亡的药物方案可能会增强抗肿瘤效果。在用他莫昔芬(TMX)联合钙调蛋白拮抗剂三氟拉嗪(TFP)或W7处理的雌激素受体阳性和阴性乳腺癌细胞培养物中,观察到了快速且强烈的凋亡诱导现象。单独使用TMX(1 - 5微摩尔)或单独使用钙调蛋白拮抗剂均未诱导凋亡。重要的是,TMX和TFP在源自原发性人类乳腺癌的细胞中也诱导了强烈的凋亡。抑制Ca2+钙调蛋白信号通路是激活上皮细胞凋亡性死亡的有效方法。TMX与无毒钙调蛋白抑制剂联合使用可能会提高TMX的预防和治疗效果。