Trichosanthes dioica seed lectin inhibits Ehrlich ascites carcinoma cells growth in vivo in mice by inducing G0/G1 cell cycle arrest.

Trichosanthes dioica seed lectin (TDSL), having a molecular mass of 57 ± 2 kDa was purified in an alternative way. For the purification process, the galactose–sepharose‐4B affinity column was used. The purified TDSL agglutinated human and mouse erythrocytes at the minimum concentration of 8 μg/ml. d‐lactose and d‐galactose were the most potent inhibitory sugars as observed. The purified lectin was a glycoprotein having 3.0% of a neutral sugar. The lectin exhibited maximum activity up to 60°C and pH range from 7.0 to 10.0 and stable up to 4.0 M urea as tested. The lectin demonstrated mild toxicity when administered against brine shrimp nauplii, and the LC50 value was calculated to be 84.0 µg/ml. Minimum agglutination of Ehrlich ascites carcinoma (EAC) cells caused by the lectin was found at the protein concentration of 1.56 µg/ml. TDSL inhibited 7, 50.2%, and 60.3% of the EAC cells growth in vivo in mice when administered with 0.75, 1.5, and 3.0 mg kg−1 day−1 (i.p.), respectively, for five consecutive days. After lectin treatment, red blood cell (RBC) and hemoglobin levels were increased significantly toward the normal compared with EAC cells‐bearing control and normal mice. The tumor burden reduced to 29.5% and 67% after treatment with 1.5 and 3.0 mg kg−1 day−1 of the lectin. TDSL triggered the cell cycle arrest at the G0/G1 phase, which was observed using flow cytometry. In conclusion, TDSL can be a candidate for the potent anticancer agents that exerts low toxicity toward brine shrimp nauplii. Practical applications: A 57 ± 2 kDa lectin (designated TDSL) was purified from Trichosanthes dioica seeds using a galactose–sepharose‐4B affinity column. The lectin demonstrated mild toxicity and agglutinated Ehrlich ascites carcinoma (EAC) cells. The lectin inhibited 50.2% and 60.3% of the EAC cell growth in vivo in mice when administered with 1.5 and 3.0 mg kg−1 day−1 (i.p.), respectively, for five consecutive days. The lectin increased RBC and hemoglobin level toward the normal compared with lectin‐treated EAC cells‐bearing, EAC cells‐bearing control and normal mice. The tumor burden reduced to 29.5% and 67% after treatment with 1.5 and 3.0 mg kg−1 day−1 lectin. TDSL triggered the cell cycle arrest at the G0/G1 phase. The lectin can be a candidate for potent anticancer agents. [ABSTRACT FROM AUTHOR]

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