|
Evaluation of Beclin 1 and Atg10 gene expression of the autophagy pathway
in acute lymphoblastic leukemia patients
|
Seyede zahra Hasanpour1    , Mehdi Allah bakhshian farsani1 , Abbas Hajifathali1 , Mohammad hossein Mohammadi 2 |
1- Shahid Beheshti University of Medical Sciences
2- Shahid Beheshti University of Medical Sciences , drmohammadi@sbmu.ac.ir |
|
|
Abstract: (4064 Views) |
Background and Aim: Acute lymphoblastic leukemia is the most common cancer in children and juveniles and is also seen in adults with lower frequency. Autophagy is a programmed catabolic process of the cell for destruction of damaged organs and proteins which is carried out by lysozymes. Disruption of autophagy leads to abnormalities in cellular processes associated with cancer.
Materials and Methods: In this study, we compared the expression of Beclin 1 and Atg 10 genes between 50 patients with B-ALL and 18 healthy subjects as our control group, by using RNA extraction and cDNA synthesis, and RT-PCR method. Data were analyzed by statistical tests.
Results: The majority of B-ALL patients showed a significant reduction in the Beclin1 and Atg 10 genes compared to control group (P <0.05) and the mean expression of the genes (2 -∆Ct ± SD) were 0.10 ± 0.49 and 1.01 ± 0.27 for ALL patients and control group and 0.15±0.44 and 1.07±0.85 for Atg10 and Beclin1 respectively. There was no significant correlation between expression levels of Beclin1and Atg10 in these patients (r =-0.013, P =0.926).
Conclusion: Considering the reduced expression levels in the essential genes of autophagy in ALL patients in our study and also other studies in this field, disruption of autophagy may be involved in leukomogensis |
|
| Keywords: Acute lymphoblastic leukemia, Autophagy, Gene expression, Beclin1, Atg 10, RTPCR |
|
|
Full-Text [PDF 801 kb]
|
Full Text (HTML)
(2705 Downloads)
|
Type of Study: Original Research |
Subject:
General
Received: 2017/12/14 | Accepted: 2019/03/24 | Published: 2019/03/24
|
|
|
|
|
|
|
| Send email to the article author |
|
|
|
| Add your comments about this article |
|
|
|
