Geodorum densiflorum rhizome lectin inhibits Ehrlich ascites carcinoma cell growth by inducing apoptosis through the regulation of BAX, p53 and NF-κB genes expression.

A lectin with a molecular mass of 12 ± 1 kDa was isolated for the first time from Geodorum densiflorum (Lam.) rhizome (GDL). The lectin exhibited hemagglutination activity both in mice and human erythrocytes which was inhibited by 4-nitrophenyl-β-D-glucopyranoside among the tested 26 sugars. The lectin was heat stable and showed its full activity in the pH range from 5.0 to 9.0. The lectin did not lose its activity in the presence of urea but the activity lost significantly when treated with EDTA. Divalent cation Ca2+ and Mg2+ also partially inhibited the activity of the lectin. The lectin strongly agglutinated Ehrlich ascites carcinoma (EAC) and inhibited the cells growth by 60% at 160 μg/ml protein concentration but unable to inhibit the growth of HeLa cells in vitro. The growth inhibition was due to the induction of apoptosis in the EAC cells which was confirmed by annexin-V and caspase-3 substrate and finally by apoptosis-related genes expression. An intensive expression of anti-apoptotic Bcl-X gene was observed only in untreated EAC cells while pro-apoptotic Bak and Bax genes expressed only in GDL treated EAC cells with the remarkable increase of the p53 gene expression. In the treated EAC cells NFκB expression was down regulated.