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Epigambogic acid, C-2 epimer of gambogic acid, inhibit cell proliferation mediated ER stress induction in HeLa cells
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Cancer Science & Therapy

ISSN: 1948-5956

Open Access

Epigambogic acid, C-2 epimer of gambogic acid, inhibit cell proliferation mediated ER stress induction in HeLa cells


5th Asia-Pacific Summit on Cancer Therapy

July 20-22, 2015 Brisbane, Australia

Aungkana Krajarng1, Masaya Imoto2, Etsu Tashiro2 and Ramida Watanapokasin3

Posters Accepted Abstracts: J Cancer Sci Ther

Abstract :

Endoplasmic reticulum (ER) plays an important role in the maintain of intracellular calcium homeostasis, protein synthesis, posttranslational modifications and protein folding. Recently, the potential of ER stress in tumor is considered important for regulating the balance between tumor cell death and growth, and for developing the sensitivity of chemotherapeutic agents. Epigambogic acid (EGA) is C-2 epimer of gambogic acid (GA), the main active ingredient in gamboge. The gamboge is a yellowish to orange dry resin secreted from Garcinia hanburyi, a plant that mainly grows in Southeast Asia, India and China. It is traditionally used as a coloring material for painting and has been also used as a folk medicine for an internal purgative and externally infected wound. Most studies demonstrated that GA had potent anti-cancer effects on a broad range of human cancer but no report about the effect of EGA. Therefore, this is the first study of anti-cancer associated ER stress induction effect of EGA on HeLa cells. The results suggest that EGA inhibited the proliferation of HeLa cells by MTT assay. EGA also induced ER stress by the up-regulation of spliced XBP1 mRNA and activated GRP78, CHOP, GADD34 and ERdj4 expression using real-time RT-PCR analysis. Comparing to our previous study, both epimers, GA and EGA, exhibited similar activities against HeLa cells. Overall, these observations might suggest that EGA inhibit cancer cell proliferation via ER stress induction which could be a novel strategy for enhancing chemotherapeutic effect of EGA as an anti-cancer agent.

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