OnLine Journal of Biological Sciences

Relative Transcription Expression Level of SIRT1, SIRT2 and SIRT3 in Correlation to the Expression of a Set of Selected Cancer Related Genes in Human Breast Cancer

Hamdy Swelim, Omnia Mansour, Salah Abdel-Rahman, Mohamed Shwaireb and Amani Kazem

DOI : 10.3844/ojbsci.2018.147.157

OnLine Journal of Biological Sciences

Volume 18, Issue 2

Pages 147-157


Mammalian Sirtuins have been shown to perform distinct cellular functions and deregulated expression of these genes was reported to be involved in the development of various malignancies including breast cancer. An increasing number of evidence indicates that Sirtuins have both tumor promoter and tumor suppressor functions. However, the roles of Sirtuins have not been well-studied in breast cancer. In the present study, quantitative expression levels of Sirtuins (SIRT1-3) together with a set of cancer related genes (cMYC, P53, SOD and HIF-1α genes) were assessed in malignant breast cancer and non-malignant control samples by using a high-throughput real-time PCR method. As a result, Sirtuins were found to be differentially expressed in breast cancer tissues and control samples, respectively. Particularly, expressions of SIRT1 (p = 0.035) and SIRT3 (p = 0.033) were found to be significantly up regulated, whereas SIRT2 (p = 0.032) gene was shown to be downregulated in breast cancer tissues compared to control samples in our study. Additionally, the expression levels of SIRT1-3 genes were correlated to both the selected cancer related genes and to clinicopathological parameters of breast cancer patients. In conclusion, SIRT1 and SIRT3 genes may act as oncogenes, whereas SIRT2 gene may operate as a tumor suppressor gene in human breast cancer.


© 2018 Hamdy Swelim, Omnia Mansour, Salah Abdel-Rahman, Mohamed Shwaireb and Amani Kazem. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.