Open AccessEffect of nicotine alkaloid extract of Nicotiana tabacum L. on the gene expression of heat shock proteins and apoptosis encoding genes in MCF-7 and Hela cancer cell lines
Author(s) -
Amenah Khudhair Khalaf,
Ibrahim Hadi Mohammed
Publication year - 2022
Publication title -
international journal of health sciences (ijhs) (en línea)
Language(s) - English
Resource type - Journals
eISSN - 2550-6978
pISSN - 2550-696X
DOI - 10.53730/ijhs.v6ns2.6395
Subject(s) - nicotiana tabacum , propidium iodide , heat shock protein , apoptosis , nicotine , biology , microbiology and biotechnology , cancer cell , mcf 7 , chemistry , programmed cell death , gene , cancer , biochemistry , genetics , human breast , neuroscience
Nicotiana tabacum L contains a many active compounds such as Nicotine, which have anti-cancer activities. Apoptosis is a regulated mechanism, and the main feature of it is activating of caspase-9. Also, heat shock proteins overexpression leads to the development of cancer. The current study is aimed to investigate the effect of Nicotine extract at IC50 (450, 75) µg\ml on the expression of the (Heat shock protein70, Hypoxia-inducing factor, P53, B-cell lymphoma-2-Associated-X-protein, and Caspase-9) in cancer cell lines, and observation the morphological changes. The quantitative Real-Time Polymerase Chain Reaction is used to analysis of gene expression by using A Kapa syber green stain, and the Acridine Orange\ Propidium iodide stain also used to observe the morphological changes. The results of this study showed that the treatment of cells with Nicotine extract at IC50 inhibits the expression of heat shock proteins encoding genes and increased the expression of apoptosis encoding gene. Also, many morphological changes was observed in apoptotic cells. The study concluded that the extract of Nicotine alkaloid of Nicotiana tabacum L. can induce the apoptosis and inhibit the expression of heat shock proteins in cancer cells making this plant is a promising option for cancer treatment, but need more research.