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Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer

✍ Scribed by Ssu-Ming Huang; Chi-Wai Cheung; Chih-Shiang Chang; Chih-Hsin Tang; Ju-Fang Liu; Yu-Hsin Lin; Jia-Hong Chen; Shihi-Hsun Ko; Dr. Kar-Lok Wong; Dr. Dah-Yuu Lu

Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
466 KB
Volume
112
Category
Article
ISSN
0730-2312

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✦ Synopsis

Abstract

This study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6‐bis(3‐chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT‐116, SW480, and Caco‐2 cells, but not in primary human dermal fibroblast cells. MCPP‐induced concentration‐dependent apoptotic cell death in colon cancer cells was measured by fluorescence‐activated cell sorter (FACS) analysis. Treatment of HCT‐116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up‐regulation of CCAAT/enhancer‐binding protein homologous protein (CHOP) and glucose‐regulated protein (GRP)‐78, phosphorylation of eukaryotic initiation factor‐2α (eIF‐2α), suggesting the induction of ER stress. MCPP also increased GSK3α/β(Tyr270/216) phosphorylation and reduced GSK3α/β(Ser21/9) phosphorylation time‐dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP‐mediated cell apoptosis. Treatment of MCPP also increased caspase‐7, caspase‐9, and caspase‐3 activity. The inhibition of caspase activity by z‐DEVE‐FMK or z‐VAD‐FMK significantly reduced MCPP‐induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP‐induced GRP and CHOP up‐regulation, and pro‐caspase‐3 and pro‐caspase‐9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3α/β activation in mediating the MCPP‐induced human colon cancer cell apoptosis. J. Cell. Biochem. 112: 643–652, 2011. © 2010 Wiley‐Liss, Inc.

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