Garlic, Ginger and Tumeric Extracts Alter Cell Cycle Arrest through Estrogen Pathway

Abstract

Garlic (Allium sativum), ginger (Zingiber officinale)) and turmeric (Curcuma longa) possess diverse nutritional, gastronomic and therapeutic functions. The effects of administration of aqueous garlic and ginger extracts, and acetone extract of tumeric at different concentrations from 4.88–1,250μg/ml were tested against the human (MCF‐7) adenocarcinoma breast cancer cell line. The phytochemical examination of these plants showed the presence of alkaloids, flavonoids, and phenol in the plant extracts, while tannins were present in garlic and ginger extracts. Terpenoids was present in garlic and turmeric extracts, cardiac glycoside was present in ginger and turmeric, steroid and saponin were exclusively present in turmeric, while anthroquinone was not detected. The radical scavenging properties of extracts were examined against 2,2‐Diphenyl‐1‐Picrylhydrazyl, Nitric Oxide (NO) and reducing power assay show significant antioxidant activity in all plant extracts along the concentration gradient. Gas chromatography‐mass spectrometry screening of the extracts identifies various biomolecules that might be responsible for anti‐carcinogenicity. The percentage viability of human adenocarcinoma breast cancer cell line (MCF‐7) was determined using MTT test, the percentage viability of cell increase across all concentrations (4.88–1250μg/ml) above 100% original viability. Cisplatin (standard drug) used as a control increase in the same pattern parallel to the garlic extract increase from 0.98 to 250 μg/ml. This result suggests that the effects of garlic, ginger and turmeric extracts do not significantly inhibit carcinogenesis / pathogenesis of human breast cancer rather promote proliferation of breast cancer cell probably due to it lower concentration of the extract that cannot effectively act on the oncogene/tumour suppressor, cyclins E and D1, and p27 of the cell. Data of study indicate that garlic, gingrer and turmeric extracts allow free promotion of the estrogen stimulation that leads to increase cellular proliferation via upregulation of cyclin D1 levels and CDK4/6 activity, as well as c‐myc, and cyclin E/CDK2 levels.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.