Methylation Status of SMG1 Gene Promoter in Multiple Myeloma
Authors
Abstract:
Background: Epigenetic modifications, such as methylation can occur in multiple myeloma. SMG1is an important gene involved in cell growth which defect in methylation of its promoter leads to reduction of cell apoptosis and uncontrolled proliferation. In this study, we identified the methylation status of the SMG1 gene promoter in patients with multiple myeloma. Methods: Methylation status of SMG1 promoter in 9 patients with multiple myeloma and 4 healthy subjects as control was determined by Methylation-specific PCR (MSP) method. Results: SMG1 promoter in all myeloma patients was hemi-methylated. Meanwhile, in healthy subjects, two cases were hemi-methylated and the other two were normal. Conclusion: The results of this study indicated that the prevalence of SMG1 promoter methylation in patients with multiple myeloma was higher than general population which could be important in understanding the pathogenesis of the disease.
similar resources
Analysis of SEPT9 Gene Promoter Methylation Status in Esophageal Squamous Cell Carcinoma
Introduction: The changes in the level of SEPT9 gene promoter methylation can contribute to the formation of esophageal squamous cell carcinoma. The aim of this study was to evaluate the level of changes in the level of SEPT9 gene promoter methylation in the esophageal squamous cell carcinoma. Methods: In the present case-control study, we collected 75 paraffin blocks of esophageal cancer tiss...
full textPCSK9 Associated Promoter Methylation Status in Patients with Hyperlipidemia
Background and purpose: Hyperlipidemia is one of the main risk factors for coronary artery disease and is defined as abnormal elevation of lipids or lipoproteins in the blood. Pcsk9 is the ninth member of the proprotein convertase family that binds to the LDLR on the surface of the hepatocyte, leading to degradation of LDLR in lysosomes which could cause hyperlipidemia. The present study aimed...
full textEpigenetic inactivation of ADAMTS9 via promoter methylation in multiple myeloma.
A disintegrin‑like and metalloprotease with thrombospondin type Ⅰ motifs (ADAMTS) are a family of 19 secreted mammalian metalloproteases. ADAMTS9 was reported to be a novel tumor suppressor gene and is downregulated in various types of human cancer due to hypermethylation of promoter CpG islands. In the present study, the silencing mechanism of th...
full textABCG2 expression, function, and promoter methylation in human multiple myeloma.
We investigated the role of the breast cancer resistance protein (BCRP/ABCG2) in drug resistance in multiple myeloma (MM). Human MM cell lines, and MM patient plasma cells isolated from bone marrow, were evaluated for ABCG2 mRNA expression by quantitative polymerase chain reaction (PCR) and ABCG2 protein, by Western blot analysis, immunofluorescence microscopy, and flow cytometry. ABCG2 functio...
full textGene Expression Status and Methylation Pattern in Promoter of P15INK4b and P16INK4a in Cord Blood CD34+ Stem Cells
Objective(s): Stem cell differentiation into different cell lineages depends upon several factors, cell cycle control elements and intracellular signaling elements, including P15INK4b and P16INK4a genes. Epigenetics may be regarded as a control mechanism which is affected by these factors with respect to their promoter structure. Materials and Methods: The CD34 + cord blood s...
full textPromoter methylation of the bone morphogenetic protein 6 gene in multiple myeloma.
Bone morphogenetic proteins (BMPs), which belong to the transforming growth factor-β superfamily, are multifunctional signaling molecules that have become of increasing interest in cancer research. Recent observations suggest that alterations in BMPs and BMP signaling are associated with tumorigenesis and disease progression in various types of ma...
full textMy Resources
Journal title
volume 10 issue 4
pages 114- 116
publication date 2018-12
By following a journal you will be notified via email when a new issue of this journal is published.
Hosted on Doprax cloud platform doprax.com
copyright © 2015-2023