Zhi-Hui Zhang1, Xin-Yue Lian2, Xi-Xi Li3, Ping-Fang He4, Jiang Lin4, Jun Qian5. 1. Central Laboratory, Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China,Department of Hematology,Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China,Department of Geriatrics, The Second Affiliated Hospital of Soochow University, Suzhou 215004, Jiangsu Province, China. 2. Central Laboratory, Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China,Department of Hematology,Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China. 3. Central Laboratory, Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China,Department of Hematology,Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China,Department of Hematology, The Second Affiliated Hospital of Soochow University, Suzhou 215004, Jiangsu Province, China. 4. Central Laboratory, Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China. 5. Central Laboratory, Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China,Department of Hematology,Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, Jiangsu Province, China,E-mail: qianjun0007@hotmail.com.
Abstract
OBJECTIVE: To investigate the clinical significance of SCIN gene expression and promoter methylation in patients with chronic myeloid leukemia (CML). METHODS: Real-time quantitative PCR was used to detect the expression level of SCIN in mononucleatr cells of bone marrow samples from 64 CML patients and 37 controls. The methylation levels of SCIN promoter in 65 patients with CML and 29 controls were detected by real-time quantitative methylation-specific PCR and bisulfite sequencing PCR. RESULTS: The expression level of SCIN in CML patients was significantly down-regulated (P＜0.05), compared with the control group. The down-regulation rate of SCIN expression in CML patients at chronic phase, accelerated phase and blast crisis was 61%, 67% and 75%, respectively. Spearman correlation analysis showed that the expression level of SCIN negatively correlated with the transcript level of BCR-ABL1 (R=-0.315, P＜0.05). However, there was no significant difference in clinical parameters such as sex, age, white blood cell count, hemoglobin level, platelet count, chromosome, CML staging and BCL-ABL1 transcript level between low and high SCIN expression groups of CML patients (P＞0.05). No significant difference in methylation of SCIN promoter between CML patients and controls, and no correlation between SCIN expression and promoter methylation were observed (P＞0.05). CONCLUSION: The SCIN expression is down-regulated in CML patients, which may relate with the pathogenesis that is, BCR-ABL1 fusion gene induces CML tumorigenesis. The down-regulation of SCIN expression may relate with the progression of CML.
OBJECTIVE: To investigate the clinical significance of SCIN gene expression and promoter methylation in patients with chronic myeloid leukemia (CML). METHODS: Real-time quantitative PCR was used to detect the expression level of SCIN in mononucleatr cells of bone marrow samples from 64 CMLpatients and 37 controls. The methylation levels of SCIN promoter in 65 patients with CML and 29 controls were detected by real-time quantitative methylation-specific PCR and bisulfite sequencing PCR. RESULTS: The expression level of SCIN in CMLpatients was significantly down-regulated (P＜0.05), compared with the control group. The down-regulation rate of SCIN expression in CMLpatients at chronic phase, accelerated phase and blast crisis was 61%, 67% and 75%, respectively. Spearman correlation analysis showed that the expression level of SCIN negatively correlated with the transcript level of BCR-ABL1 (R=-0.315, P＜0.05). However, there was no significant difference in clinical parameters such as sex, age, white blood cell count, hemoglobin level, platelet count, chromosome, CML staging and BCL-ABL1 transcript level between low and high SCIN expression groups of CMLpatients (P＞0.05). No significant difference in methylation of SCIN promoter between CMLpatients and controls, and no correlation between SCIN expression and promoter methylation were observed (P＞0.05). CONCLUSION: The SCIN expression is down-regulated in CMLpatients, which may relate with the pathogenesis that is, BCR-ABL1 fusion gene induces CML tumorigenesis. The down-regulation of SCIN expression may relate with the progression of CML.