Anticancer drugs induce cell death mechanism in tumor cells by various modes, which include apoptosis, autophagy, and necroptosis. However, they become ineffective when tumor cells enter metastasis. Thus, searching for plantbased extracts/compounds to curtail metastasis is extremely important. This study aims to evaluate the anticancer potential of Tamarix articulata (TA) extract against prostate cancer cells. MTT, Brd U, and trypan blue assays were carried out to evaluate the cell viability. Terminal Transferase dUTP Nick End Labeling assay was carried out to determine apoptotic cells. Clonogenic, wound-healing, and Boyden chamber assay was conducted to evaluate the anticlonogenic, antimotility, and anti-invasive potential of TA. Zymography and immunoblotting were carried out to check the activity and expression of metalloproteases and proteins associated with metastasis. Our results demonstrated that TA extract significantly inhibits cell viability and clonogenic property and displays IC50 values in the 245289 µg/ml range. TA extract significantly abrogates the motility and invasive property of LnCaP cells in a dose-dependent manner. Mechanistically, TA extracts downregulate the expression of phosphoinositide 3-kinaseprotein kinase B-protein kinase B (PI3K-Akt), transforming growth factor-beta-Sma genes and the Drosophila Mad, mothers against decapentaplegic protein 2/3 (TGF-β-SMAD2/3), and matrix metalloproteinases-2/9 (MMP-2/9) with concomitant upregulation of tissue inhibitor of metalloproteinase 1 (TIMP1) expression in LnCaP cells. Additionally, we observed a dose-dependent downregulation of snail and vimentin with the upregulation of E-cadherin protein expression in LnCaP cells. TA extract exhibits an antiproliferative effect and abrogates cell motility and invasion by downregulating PI3K-Akt, TGF-β-SMAD2/3, MMP-2/9, snail, and vimentin with concomitant upregulation of E-cadherin and TIMP1 expression in prostate cancer cells.
Key words: Tamarix articulata; plant extracts; metastasis; anticancer; prostate cancer; apoptosis; cell motility; cell invasion.
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