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

Research paper by A K M AKM Asaduzzaman, Imtiaj I Hasan, Aninda A Chakrabortty, Sadnima S Zaman, Shaikh Shohidul SS Islam, Fazle Rabbi Shakil FRS Ahmed, K M Ahsanul KMA Kabir, Md M Nurujjaman, Md Belal MB Uddin, Mohammad Taufiq MT Alam, Ranajit Kumar RK Shaha, Syed Rashel SR Kabir

Indexed on: 19 Oct '17Published on: 19 Oct '17Published in: International Journal of Biological Macromolecules


A Moringa oleifera seed lectin (MOSL) was purified by using chitin column with the molecular mass of 17±1kDa. The lectin agglutinated mouse, cow and human erythrocytes and the hemagglutination activity was inhibited by methyl-α-D-mannopyranoside, methyl-β-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°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 131.0μg/ml. Antiproliferative activity was studied against Ehrlich ascites carcinoma (EAC) cells and 71.08% cell growth inhibition was observed in vitro at 200μg/ml. The lectin was injected (i.p.) into EAC mice at the doses of 2.0 and 4.0mg/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 G2/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-κB genes expression.