caa a22 4500 606234209 CHVBK 20210128101236.0 cr unu---uuuuu 210128e20150101xx s 000 0 eng 10.1007/s11010-014-2257-2 doi (NATIONALLICENCE)springer-10.1007/s11010-014-2257-2 Ellagic acid inhibits proliferation and induced apoptosis via the Akt signaling pathway in HCT-15 colon adenocarcinoma cells [Elektronische Daten] [Syed Umesalma, Ponnuraj Nagendraprabhu, Ganapasam Sudhandiran] Chemoprevention is regarded as one of the most promising and realistic approaches in the prevention of human cancer. Ellagic acid (EA) has been known for its chemopreventive activity against various cancers and numerous investigations have shown its apoptotic activity both in vivo and in vitro. The present study was focused to elucidate the anticancerous effect and the mode of action of EA against HCT-15 colon adenocarcinoma cells. Cell viability was assessed using trypan blue assay at different concentrations. EA also promoted cell cycle arrest substantially at G2/M phase in HCT-15 cells. The activities of alkaline phosphatase and lactate dehydrogenase were decreased upon EA treatment, which shows the antiproliferative and the cytotoxic effects, respectively. The production of reactive oxygen intermediates, which were examined by 2,7-dichlorodihydrofluorescein diacetate (H2DCF-DA), increased with time, after treatment with EA. In further studies, EA inhibited proliferation-associated markers proliferating cell nuclear antigen and cyclin D1. The induction of apoptosis was accompanied by a strong inactivation of phosphatidylinositol 3-kinase (PI3K)/Akt pathway by EA. The expression of PI3K and pAkt was down-regulated in EA-treated cells, compared to normal cells. Further, EA promoted the expression of Bax, caspase-3, and cytochrome c, and suppression of Bcl-2 activity in HCT-15 cells that was determined by western blot analysis. Increased annexin V apoptotic cells and DNA fragmentation also accompanied EA-induced apoptosis. In conclusion, EA increased the production of ROS, decreased cell proliferation, and induced apoptosis in HCT-15 cells, and thus can be used as an agent against colon cancer. Springer Science+Business Media New York, 2014 Colon cancer nationallicence HCT-15 cells nationallicence Ellagic acid nationallicence Proliferation nationallicence A poptosis nationallicence Akt pathway nationallicence Umesalma Syed Department of Biochemistry, Cell Biology Unit, University of Madras, Maraimalai Campus (Guindy), 600 025, Chennai, Tamil Nadu, India aut Nagendraprabhu Ponnuraj Department of Biochemistry, Cell Biology Unit, University of Madras, Maraimalai Campus (Guindy), 600 025, Chennai, Tamil Nadu, India aut Sudhandiran Ganapasam Department of Biochemistry, Cell Biology Unit, University of Madras, Maraimalai Campus (Guindy), 600 025, Chennai, Tamil Nadu, India aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 399/1-2(2015-01-01), 303-313 0300-8177 399:1-2<303 2015 399 11010 https://doi.org/10.1007/s11010-014-2257-2 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-014-2257-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Umesalma Syed Department of Biochemistry, Cell Biology Unit, University of Madras, Maraimalai Campus (Guindy), 600 025, Chennai, Tamil Nadu, India aut NATIONALLICENCE 700 1- Nagendraprabhu Ponnuraj Department of Biochemistry, Cell Biology Unit, University of Madras, Maraimalai Campus (Guindy), 600 025, Chennai, Tamil Nadu, India aut NATIONALLICENCE 700 1- Sudhandiran Ganapasam Department of Biochemistry, Cell Biology Unit, University of Madras, Maraimalai Campus (Guindy), 600 025, Chennai, Tamil Nadu, India aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 399/1-2(2015-01-01), 303-313 0300-8177 399:1-2<303 2015 399 11010