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العنوان
Expression of microRNA-96 and it relationship to matrix metalloproteinase regulator- RECK in Retinoblastoma /
المؤلف
Ibrahim, Mohamed Ibrahim Mohamed Aziz.
هيئة الاعداد
باحث / محمد ابراهيم عزيز ابراهيم
مشرف / عزة حسن ابوغالية
مشرف / عزة محمد أحمد
مشرف / مروة على عبد الخالق
تاريخ النشر
2019.
عدد الصفحات
159 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الكيمياء الحيوية (الطبية)
تاريخ الإجازة
1/1/2019
مكان الإجازة
جامعة عين شمس - كلية الطب - الكيمياء الحيوية الطبية والبيولوجيا الجزيئية
الفهرس
Only 14 pages are availabe for public view

from 159

from 159

Abstract

Retinoblastoma is a childhood malignant tumor of the retinoblasts, with prevalence rate 1:15,000–1:20,000. It may occur in non-heritable (70%–75%) or heritable (25%–30%) forms. That malignancy is due to a mutation occurred in the retinoblastoma gene (RB1), a tumor suppressor gene that is located on chromosome 13.
Micro RNAs play a major role in tumorigenesis of many malignancies mainly by activating an oncogenic gene or silencing a tumor suppressor gene by targeting its mRNA for destruction.
Mir- 96 was identified as an oncogenic micro-RNA in many malignancies as breast cancer, lung cancer and colon cancer. It induces malignant cells proliferative and invasive abilities by targeting many putative tumor suppressors as FOXO3a and RECK.
RECK is a human gene that act as metastasis suppressor. This gene codes for a glycoprotein that contains cysteine rich and protease inhibitor-like domains. The RECK protein suppresses tumor invasion, angiogenesis and metastasis by downregulating matrix metalloproteinases (MMP-2, MMP-9 and MT1-MMP). Many studies reported RECK mRNA as a target of miR-96 in many cancers.
This study aimed at evaluating the expression of miRNA-96 in some patients with retinoblastoma and its relationship to the level of the matrix metalloproteinase regulator- RECK, in order to give insights on their possible role as potential biomarkers in retinoblastoma.
The current study involved patients group that included 14 children with recently diagnosed retinoblastoma, and control group included 14 children with eye diseases other than retinoblastoma matching the patient group for age and sex. The patients with retinoblastoma were once re-evaluated 6 months after receiving 1st session of treatment. Patients who were on chemotherapy or radiotherapy at the beginning of the study were excluded from the study.
Three milliliters of peripheral blood samples were taken from the included children, and sera were obtained and then stored at -80 C until laboratory analysis. The following assays were performed:
a. The expression level of micro RNA-96 were examined using quantitative reverse transcription qRT-PCR.
b. RECK protein was measured in serum samples by ELISA technique.
The statistical analysis of the results indicated that the expression of miR- 96 was significantly higher in the sera of patients than the control group (P<0.05). The concentration of RECK protein was significantly decreased in the patients compared to control group (P<0.05). Furthermore, the level of miR- 96 was significantly decreased (P<0.05), and concentration of RECK protein was significantly increased (P<0.05) in the sera after treatment in patients who responded to globe salvage treatment. Moreover the expression of RECK protein, and miR- 96 was negatively correlated with each other in the patients before treatment as well as after treatment and in the control group.
In conclusion, serum level of miR-96 and RECK protein concentration may serve as potential biomarkers in retinoblastoma.