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Moringa oleifera seed lectin inhibits Ehrlich ascites carcinoma cell growth by inducing apoptosis through the regulation of Bak and NF-κB gene expression

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DOI: 10.1016/j.ijbiomac.2017.10.070

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Apoptosis; Cell cycle; Gene expression

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A Moringa oleifera seed lectin (MOSL) was purified by using chitin column with the molecular mass of 17 +/- 1 kDa. The lectin agglutinated mouse, cow and human erythrocytes and the hemagglutination activity was inhibited by methyl-alpha-D-mannopyranoside, methyl-beta-D-galactopyranoside, lactose and glucose. The lectin exhibited 100% hemagglutination activity at the pH range from 8.0 to 9.0 and temperature range from 30 to 60 degrees C. Additionally, the lectin gradually lost its activity in the presence of urea but the activity abolish completely when treated with EDTA. MOSL showed mild toxicity against brine shrimp nauplii with a LC50 value of 131.0 mu g/ml. Antiproliferative activity was studied against Ehrlich ascites carcinoma (EAC) cells and 71.08% cell growth inhibition was observed in vitro at 200 mu g/ml. The lectin was injected (i.p.) into EAC mice at the doses of 2.0 and 4.0 mg/kg/day for five consecutive days and 25.38% and 55% of cell growth inhibition was observed, respectively. MOSL caused the cell cycle arrest at G(2)/M phase as determined by FACS flow cytometry. The cell growth inhibition was due to the induction of apoptosis in the EAC cells which was confirmed by cell morphological study, caspase-3 inhibitor and activation of Bak and suppression of Bcl-2 and NF-kappa B genes expression. (C) 2017 Elsevier B.V. All rights reserved.

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