Manal Almalky
King Saud university Riyadh, Saudi Arabia
Title: The synergistic effect of melatonin and vitamin D3 on the gene expression of Bcl-2 and Bax in MCF-7 breast cancer cell line
Biography
Biography: Manal Almalky
Abstract
There is now compelling evidence by epidemiology and experimental studies that disruption of circadian rhythm and decreased melatonin synthesis is a risk factor for the breast cancer. Also interestingly there is a strong co-relationship between the night shift work and the incidence of breast cancers. Animal model of cancer suggests that the disruption of light and night (LAN) disrupts the secretion of melatonin and enhances the growth of chemical induced mammary adenocarcinoma in comparison with the control animals. The use of melatonin along with tamoxifen greatly increase the efficacy of the drug as well as better strategy to treat breast cancers, which are now used in some clinical studies. Similarly, the use of melatonin and vitamin D3 has shown to inhibit breast cancer growth and promote apoptosis. With the ever increasing rate of breast cancer incidences there is a strong need to look at the alternative drugs and treatment strategy for the treatment of breast cancer. There is also a need for the better understanding of how these drugs may affect the tumour cell apoptosis and control of metastasis. Our in-vitro results with breast cancer cell line MCF-7 showed that the synergistic treatment of vitamin D3 and melatonin can upregulate pro-apoptotic Bax gene expression as well as protein expression as shown by RTPCR and immunoblotting techniques and at the same time downregulating the gene expression and protein expression of anti-apoptotic gene BCl-2. BCL-2/Bax ratio usually determines the extent to which apoptosis is induced or suppressed. Our gene expression and immunoblotting data supports the notion that melatonin and vitamin D3 susceptible apoptosis is induced by significantly suppressing BCL-2 expression with concombitant upregulation of Bax gene expression and protein expression.