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转变为恶性的一重要特征是调节胆固醇合成的胆固醇反馈抑制机制失控。癌细胞似乎需要存在于胆固醇和胆固醇前体浓度增加的环境中。因此,有理由假设控制已有的胆固醇或胆固醇的合成都能达到预防肿瘤生长的目的。体内和细胞培养实验显示了降低血清胆固醇浓度或用3-羟3-甲基戊二酰(HMG)辅酶A还原酶抑制剂干扰甲羟戊酸途径减慢了肿瘤的生
An important feature of the transition to malignancy is that the cholesterol feedback inhibition mechanism that regulates cholesterol synthesis is out of control. Cancer cells seem to need to be present in an environment where concentrations of cholesterol and cholesterol precursors increase. Therefore, it is reasonable to assume that controlling the existing cholesterol or cholesterol synthesis can achieve the purpose of preventing tumor growth. In vivo and cell culture experiments have shown that lowering serum cholesterol concentrations or interfering with the mevalonate pathway with 3-hydroxy-3-methylglutaryl (HMG) coenzyme A reductase inhibitors slows tumor growth