Molecular genetics & genomic medicine · 2020
Aberrant DNA methylation of PTPRG as one possible mechanism of its under-expression in CML patients in the State of Qatar.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Ismail Mohamed A, Samara Muthanna, Al Sayab Ali, Alsharshani Mohamed, Yassin Mohamed A, Varadharaj Govindarajulu, Vezzalini Marzia, Tomasello Luisa, Monne Maria, Morsi Hisham, Qoronfleh M Walid, Zayed Hatem, Cook Richard, Sorio Claudio, Modjtahedi Helmout, Al-Dewik Nader I
Аннотация
BACKGROUND: Several studies showed that aberrant DNA methylation is involved in leukemia and cancer pathogenesis. Protein tyrosine phosphatase receptor gamma (PTPRG) expression is a natural inhibitory mechanism that is downregulated in chronic myeloid leukemia (CML) disease. The mechanism behind its downregulation has not been fully elucidated yet.
AIM: This study aimed to investigate the CpG methylation status at the PTPRG locus in CML patients.
METHODS: Peripheral blood samples from CML patients at time of diagnosis [no tyrosine kinase inhibitors (TKIs)] (n = 13), failure to (TKIs) treatment (n = 13) and healthy controls (n = 6) were collected. DNA was extracted and treated with bisulfite treatment, followed by PCR, sequencing of 25 CpG sites in the promoter region and 26 CpG sites in intron-1 region of PTPRG. The bisulfite sequencing technique was employed as a high-resolution method.
RESULTS: CML groups (new diagnosed and failed treatment) showed significantly higher methylation levels in the promoter and intron-1 regions of PTPRG compared to the healthy group. There were also significant differences in methylation levels of CpG sites in the promoter and intron-1 regions amongst the groups.
CONCLUSION: Aberrant methylation of PTPRG is potentially one of the possible mechanisms of PTPRG downregulation detected in CML.
AIM: This study aimed to investigate the CpG methylation status at the PTPRG locus in CML patients.
METHODS: Peripheral blood samples from CML patients at time of diagnosis [no tyrosine kinase inhibitors (TKIs)] (n = 13), failure to (TKIs) treatment (n = 13) and healthy controls (n = 6) were collected. DNA was extracted and treated with bisulfite treatment, followed by PCR, sequencing of 25 CpG sites in the promoter region and 26 CpG sites in intron-1 region of PTPRG. The bisulfite sequencing technique was employed as a high-resolution method.
RESULTS: CML groups (new diagnosed and failed treatment) showed significantly higher methylation levels in the promoter and intron-1 regions of PTPRG compared to the healthy group. There were also significant differences in methylation levels of CpG sites in the promoter and intron-1 regions amongst the groups.
CONCLUSION: Aberrant methylation of PTPRG is potentially one of the possible mechanisms of PTPRG downregulation detected in CML.