Curcumin Downregulates the Expression of p44/42 MAPK and Causes Caspase-mediated Cell Inhibition in MCF-7 Breast Cancer Cells
Keywords:
MCF-7, Curcumin, p44/42 MAPK, caspases, cancerAbstract
Curcumin is a derivative of the turmeric spice, which is a yellow-pigmented root crop with a resilient sheath and bright orange flesh. It is originally known to be utilized in Asian dishes but, has been discovered to have antioxidant, anti-inflammatory, antiviral, antibacterial and anticancer characteristics. Different researchers have established great possibilities of curcumin's ability to prohibit the growth of cancer cells especially, because of its potentiality to differentiate between normal and cancerous cells. Research questions include understanding the effects of curcumin on the MCF-7 breast cancer cells with regards to the biomolecules of the cells. The results indicated that after attachment of cells for 48 hours, the concentration of curcumin at 15 µM showed more than 90% inhibition of cells within 24 hours. The analysis was carried out on the viability of the cells, western blotting and reverse transcriptase-polymerase chain reaction. Western blot analysis of signaling proteins from curcumin-treated cells showed that the expression level of phosphorylated protein p44/42 in the MAP kinase pathway was significantly decreased and the apoptotic marker cleaved caspase 3 was increased as compared to the curcumin-untreated control cells. Moreover, RT-PCR analysis of the reference genes in the apoptotic pathway (p53, caspase 9, BCL-2 and Bax) demonstrated the upregulation of p53, Bax and caspase 9 genes. The results assembled from this present study suggested that curcumin inhibited the growth and induced caspase-mediated apoptosis of MCF-7 cells via the MAPK signaling pathway. Therefore, breast cancer treatment with curcumin seems to be a promising remedial path in near future.
Downloads
Published
How to Cite
Issue
Section
License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
Author(s) will retain the copyright of their own articles. By submitting the article to Bioresearch Communications (BRC), the author(s) have granted the BRC for the use of the article.