Batetta B, Pulisci D, Bonatesta R R, Sanna F, Piras S, Mulas M F, Spano O, Putzolu M, Broccia G, Dessì S
Istituto di Patologia Sperimentale, Cagliari, Italy.
Cancer Lett. 1999 Jun 1;140(1-2):53-8. doi: 10.1016/s0304-3835(99)00052-x.
In the present study we examined gene expression and glucose-6-phosphate dehydrogenase (G6PD) activity in leukemic cells isolated from G6PD normal and deficient subjects. The results have shown that G6PD activity strongly increases in G6PD normal leukemic cells as well as in G6PD deficient leukemic cells when compared to peripheral blood mononuclear cells (PBMC). Higher levels of G6PD gene expression were observed in leukemic cells from G6PD deficient patients compared to G6PD normal. A similar pattern of gene expression was also observed for 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase. These results support the hypothesis that G6PD deficient cell, in order to sustain their growth, must respond to the low activity of their mutant enzyme with an increase in quantity through an induction of gene expression.
在本研究中,我们检测了从葡萄糖-6-磷酸脱氢酶(G6PD)正常和缺陷受试者中分离出的白血病细胞中的基因表达和G6PD活性。结果表明,与外周血单个核细胞(PBMC)相比,G6PD正常的白血病细胞以及G6PD缺陷的白血病细胞中的G6PD活性均显著增加。与G6PD正常的患者相比,在G6PD缺陷患者的白血病细胞中观察到更高水平的G6PD基因表达。对于3-羟基-3-甲基戊二酰辅酶A(HMGCoA)还原酶,也观察到了类似的基因表达模式。这些结果支持了这样的假设,即G6PD缺陷细胞为了维持其生长,必须通过基因表达的诱导来增加数量,以应对其突变酶的低活性。