Paper Details

PJB-2020-224

ALLIUM AMPELOPRASUM L. AND ITS SELECTED BIOACTIVE CONSTITUENTS AS POTENTIAL ER INHIBITORS FOR BREAST CANCER BIOASSAY GUIDED AND PHARMACOPHORE BASED MOLECULAR DOCKING STUDIES

Sidra Rehman
Abstract

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Estradiol controls numerous physiological processes in different target tissues and involves in advancement and progression of endometrial and breast cancer. Phytochemicals act as both antagonists and agonists of estrogen receptors (ERs) of humans either by directly binding to ER or by acting on cell-specific selective ER modulators. To probe the antiproliferative and antiestrogenic activity of Pakistani medicinal plants in estrogen receptor expressing cancer cells. Different parts of eight indigenous medicinal plants were extracted in methanol and analyzed for anti-proliferative activity in human liver cancer (HepG2) and breast adenocarcinoma (MDA-MB-231) cells. For analysis of anti-estrogenic activity of medicinal plant extracts, fibroblast cells were co-transfected with pCR3.1 ER-α and pGL5 ERE-LUC plasmids in the presence and absence of methanolic extracts of medicinal plants. Allium ampeloprasum seeds (AA) and Saussurea Lappa (SL) roots extracts have shown inhibition of 60% and 44% liver tumor cells proliferation respectively. Breast carcinoma cells were suppressed in their growth when treated with A. ampeloprasum and S. lappa. A. ampeloprasum seeds extract effectively suppressed 6.3 fold E2-mediated transcriptional activity when compared with control which contained dimethylsulfoxide (DMSO) instead of plant extract. N-(γ-glutamyl)-S-(E-1-propenyl) cysteine, S-propyl-L-cysteine sulfoxide and S-methyl cysteine sulfoxide are the phytoconstituents of A. ampeloprasum which have delineated minimum binding energy and hence least docking score against ER-α as compared to Tamoxifen (control drug). Our findings demonstrated the antagonistic role of A. ampeloprasum extract and it’s phytoconstituents for human ER-α. Results of our study concluded that A. ampeloprasum potentially blocked human ER-α expression monitored by ERE-luciferase reporter assay.

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