Antitumor properties of a methyl-β-d-galactopyranoside specific lectin from Kaempferia rotunda against Ehrlich ascites carcinoma cells.

Autor: Ahmed FRS; Department of Biochemistry and Molecular Biology, Faculty of Science, University of Rajshahi, Rajshahi 6205, Bangladesh., Amin R; Bangladesh Council of Scientific and Industrial Research Laboratories, Binodpul Bazar, Rajshahi, Bangladesh., Hasan I; Department of Biochemistry and Molecular Biology, Faculty of Science, University of Rajshahi, Rajshahi 6205, Bangladesh., Asaduzzaman AKM; Department of Biochemistry and Molecular Biology, Faculty of Science, University of Rajshahi, Rajshahi 6205, Bangladesh., Kabir SR; Department of Biochemistry and Molecular Biology, Faculty of Science, University of Rajshahi, Rajshahi 6205, Bangladesh. Electronic address: rashelkabir@ru.ac.bd.
Jazyk: angličtina
Zdroj: International journal of biological macromolecules [Int J Biol Macromol] 2017 Sep; Vol. 102, pp. 952-959. Date of Electronic Publication: 2017 Apr 28.
DOI: 10.1016/j.ijbiomac.2017.04.109
Abstrakt: A lectin was isolated from the tuberous rhizome of Keampferia rotunda by using different chromatographic methods with the molecular weight of 21±1kDa. The lectin contained highest percentage of leucine and lowest percentage of tryptophan residues as determined by LC-MS. The lectin agglutinated mice and human erythrocytes and the hemagglutination activity was inhibited by Methyl-β-d-galactopyranoside. The lectin did not lose its activity in the presence of urea but the activity abolished completely when treated with EDTA. The lectin exhibited its activity at the pH ranging from 6.0 to 9.0 and in a temperature range of 30-80°C. Antiproliferative activity was studied against Ehrlich ascites carcinoma (EAC) and U87 cell lines. No inhibitory effect was observed against U87 cell line whereas 43.7% cell growth inhibition was observed in vitro against EAC cells at 160μg/ml. The lectin was injected (i.p.) in EAC bearing Swiss albino mice at the doses of 3.0 and 6.0mg/kg/day for five consecutive days and 41 and 59% of EAC cell growth inhibition was observed, respectively. 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 apoptosis-related gene expression.
(Copyright © 2017 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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