Mizani Sharareh, Keshavarz Ali, Vazifeh Shiran Nader, Bashash Davood, Allahbakhshian Farsani Mehdi
Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, P.O. Box: 15468-15514, Tehran, Iran.
Indian J Hematol Blood Transfus. 2023 Jul;39(3):392-401. doi: 10.1007/s12288-022-01612-3. Epub 2022 Dec 1.
The increased metabolism in acute myeloid leukemia (AML) malignant cells resulted in the production of high levels of free radicals, called oxidative stress conditions. To avoid this situation, malignant cells produce a considerable amount of antioxidant agents, which will lead to the release of a continuous low level of reactive oxygen species (ROS), causing genomic damage and subsequent clonal evolution. SIRT1 has a key role in driving the adaptation to this condition, mainly through the deacetylation of FOXO3a that affects the expression of oxidative stress resistance target genes such as Catalase and Manganese superoxide dismutase (MnSOD). The aim of this study is to simultaneously investigate the expression of SIRT1, FOXO3a, and free radical-neutralizing enzymes such as Catalase and MnSOD in AML patients and measure their simultaneous change in relation to each other. The gene expression was analyzed using Real Time-PCR in 65 AML patients and 10 healthy controls. Our finding revealed that expression of SIRT1, FOXO3a, MnSOD and Catalase was significantly higher in AML patients in comparison to healthy controls. Also, there was a significant correlation between the expression of SIRT1 and FOXO3a, as well as among the expression of FOXO3a, MnSOD and Catalase genes in patients. According to the results, the expression of genes involved in oxidative stress resistance was higher in AML patients, which possibly contributed to the development of malignant clones. Also, the correlation between the expression of SIRT1 and FOXO3a gene reflects the importance of these two genes in increased oxidative stress resistance of cancer cells.
急性髓系白血病(AML)恶性细胞中代谢的增加导致产生高水平的自由基,即氧化应激状态。为避免这种情况,恶性细胞会产生大量抗氧化剂,这将导致持续低水平的活性氧(ROS)释放,从而造成基因组损伤及随后的克隆进化。SIRT1在驱动对这种状况的适应中起关键作用,主要是通过使FOXO3a去乙酰化,这会影响过氧化氢酶和锰超氧化物歧化酶(MnSOD)等抗氧化应激靶基因的表达。本研究的目的是同时调查AML患者中SIRT1、FOXO3a以及过氧化氢酶和MnSOD等自由基中和酶的表达情况,并测量它们彼此之间的同步变化。使用实时定量聚合酶链反应(Real Time-PCR)对65例AML患者和10名健康对照者的基因表达进行了分析。我们的研究结果显示,与健康对照者相比,AML患者中SIRT1、FOXO3a、MnSOD和过氧化氢酶的表达显著更高。此外,患者中SIRT1和FOXO3a的表达之间,以及FOXO3a、MnSOD和过氧化氢酶基因的表达之间存在显著相关性。根据结果,AML患者中参与抗氧化应激的基因表达更高,这可能有助于恶性克隆的发展。此外,SIRT1和FOXO3a基因表达之间的相关性反映了这两个基因在癌细胞抗氧化应激能力增强中的重要性。