Evaluating the expression of LKB1, SHMT1, and GLDC genes in Acute Lymphoblastic Leukemia patients

Pegah Farajzadeh; Flora Forouzesh Postdoc; Maryam Nabigol; Mehdi Allahbakhshian Farsani

doi:10.18502/ijpho.v14i3.15991

Pegah Farajzadeh Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
Flora Forouzesh Postdoc Assistant professor, Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad university, Tehran, Iran
Maryam Nabigol Department of Hematology and Blood Bank, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Mehdi Allahbakhshian Farsani Department of Hematology and Blood Bank, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran

DOI: https://doi.org/10.18502/ijpho.v14i3.15991

Keywords: Glycine dehydrogenase , Precursor cell lymphoblastic, leukemia-Lymphoma, STK11 protein

Abstract

Background: Epigenetic changes in cancer cells have an immense effect on tumorigenesis. As a tumor suppressor and an epigenetic regulator, liver kinase B1 (LKB1) reduces gene methylation by downregulating metabolic pathways such as the serine-glycine pathway. This study seeks to examine the gene expression levels of serine hydroxymethyltransferase 1 (SHMT1) and glycine decarboxylase (GLDC), as two serine-glycine pathway regulatory genes, along with LKB1 in acute lymphoblastic leukemia (ALL) patients.

Materials and Methods: In this analytical study, qRT-PCR was used to evaluate the gene expression levels of LKB1, SHMT1, and GLDC in 50 ALL patients with an average age of 11.64 ± 10.6 years. The patients were compared to 10 healthy controls. Subsequently, the correlation between the gene expression levels and the patients’ demographic data was investigated.

Results: No significant difference was found between the ALL patients and the control individuals in terms of LKB1 and GLDC gene expressions, but SHMT1 was significantly overexpressed in the ALL patients (p = 0.003). Moreover, there was a significant association between GLDC and the other SHMT1 (p = 0.020) and LKB1 (p = 0.047). No significant connection was also found between the age (pL = 0.304, pS = 0.305, pG = 0.899), gender (pL = 0.475, pS = 0.299, pG = 0.388), and blast percentage (pL = 0.335, pS = 0.148, pG = 0.459) of the patients and the genes.

Conclusion: The increased expression of SHMT1 suggests the oncogenic role of this gene. Thus, the present study offers a novel diagnostic marker in ALL patients.