Volume 43, Issue 3 (10-2019)
Research in Medicine 2019, 43(3): 170-176 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
askari N, Shafieipour S, Aghajanpour M. Role of BAX, BCL-2, and MICAL-2 Genes in Esophageal Cancer. Research in Medicine 2019; 43 (3) :170-176
URL: http://pejouhesh.sbmu.ac.ir/article-1-1954-en.html
URL: http://pejouhesh.sbmu.ac.ir/article-1-1954-en.html
Graduate University of Advanced Technology , nahidaskari@gmail.com
Abstract: (4350 Views)
Background: Esophageal cancer is one of the most common gastrointestinal tract cancers. In cancer cells, interactions take place between apoptosis and cell proliferation and there is a positive correlation between BAX and BCL-2 genes expression levels and cancerous process. The MICAL-2 gene encodes monooxygenase enzyme which causes F-actin instability. Increasing the expression of this gene plays an important role in Epithelial-mesenchymal transition in cancerous tissue and consequently causes metastases. Since no study of MICAL-2, BAX, and BCL2 genes in esophageal cancer has been reported, the present study aimed to determine the expression of these genes in esophageal cancer patients in Kerman, Iran, in 2017-2018 using Real Time RT-qPCR.
Materials and Methods: A case-control study was designed to determine the changes in the expression level of BAX, BCL2, and MICAL-2 genes. A total of 40 samples (20 fresh tissues and 20 Paraffin Embedded tissues) and marginal non-tumor control tissues were obtained. First, total mRNAs of the samples were extracted, and then after cDNA synthesis, the expression rates of MICAL2, BAX, and BCL2 were determined using Real-Time RT-qPCR. The data were analyzed using descriptive and deductive statistic methods (Generalized Linear Models) at α < 0.05 via SPSS software (v.20).
Results: The expression levels of MICAL2 (1.2%) and BCL2 (2.04%) in patients with esophageal cancer were higher than those of normal tissues, while BAX (0.46%) gene expression in the normal tissue was higher than that of the cancerous ones. In the pathologic study, it was found that 62.5% of the samples were esophageal squamous cell carcinoma.
Conclusion: Regarding the changes in the expression of BAX, BCL2, and MICAL2 genes in esophageal cancer, for determination of the expression level in individuals who have a family history of this problem, these genes can be used as biomarkers, because the diagnosis of cancer in the early stages have definitely a better response to therapies.
Materials and Methods: A case-control study was designed to determine the changes in the expression level of BAX, BCL2, and MICAL-2 genes. A total of 40 samples (20 fresh tissues and 20 Paraffin Embedded tissues) and marginal non-tumor control tissues were obtained. First, total mRNAs of the samples were extracted, and then after cDNA synthesis, the expression rates of MICAL2, BAX, and BCL2 were determined using Real-Time RT-qPCR. The data were analyzed using descriptive and deductive statistic methods (Generalized Linear Models) at α < 0.05 via SPSS software (v.20).
Results: The expression levels of MICAL2 (1.2%) and BCL2 (2.04%) in patients with esophageal cancer were higher than those of normal tissues, while BAX (0.46%) gene expression in the normal tissue was higher than that of the cancerous ones. In the pathologic study, it was found that 62.5% of the samples were esophageal squamous cell carcinoma.
Conclusion: Regarding the changes in the expression of BAX, BCL2, and MICAL2 genes in esophageal cancer, for determination of the expression level in individuals who have a family history of this problem, these genes can be used as biomarkers, because the diagnosis of cancer in the early stages have definitely a better response to therapies.
Type of Study: Original |
Subject:
Genetic
Received: 2018/12/3 | Accepted: 2019/05/29 | Published: 2019/09/17
Received: 2018/12/3 | Accepted: 2019/05/29 | Published: 2019/09/17
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
This Journal is licensed under a Creative Commons Attribution 4.0 International License | Research in Medicine
Designed & Developed by : Yektaweb