Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/13040
Title: Etlingera elatior Extract promotes cell death in B16 melanoma cells via down-regulation of ERK and Akt signaling pathways
Authors: Krajarng A.
Chulasiri M.
Watanapokasin R.
Keywords: plant extract
protein kinase B
animal
apoptosis
cell survival
chemistry
down regulation
drug effects
MAPK signaling
metabolism
mouse
tumor cell line
Zingiberaceae
Animals
Apoptosis
Cell Line, Tumor
Cell Survival
Down-Regulation
MAP Kinase Signaling System
Mice
Plant Extracts
Proto-Oncogene Proteins c-akt
Zingiberaceae
Issue Date: 2017
Abstract: Background: Torch ginger (Etlingera elatior, EE) is a ginger plant that found in Southeast Asia. Previous study showed its flowers and leaves composed of several flavonoids with anti-cancer activity. This study aims to investigate the mechanism of EE extract on cell death induction in melanoma cells. Methods: To carry out this study, the cytotoxic effect of EE extract was performed using MTT assay. Nuclear morphological change and loss of mitochondrial membrane potential were observed using Hoechst 33,342 and JC-1 staining. Flow cytometry using Annexin V/PI double staining assessed apoptosis, necrosis and viability. Caspase activity was detected by caspase activity kits. The expression of Bcl-2 family proteins, ERK and Akt signaling pathways were examined by Western blot analysis. Results: The treatment of EE extract resulted in a dose- and time-dependent reduction in cell viability in B16 cells. It also induced nuclear condensation, phosphatidylserine exposure, and loss of mitochondrial membrane potential, which are markers of apoptosis. Furthermore, the expression of Bim was increased instead of Bax and Bcl-2. The results also showed caspase-independent activity and the down-regulation of ERK and Akt signaling pathway. Conclusion: The results suggest that EE extract induced caspase-independent cell death via down-regulation of ERK and Akt pathways in B16 cells. This may be beneficial as a chemopreventive or chemotherapeutic agent in melanoma treatment. © 2017 The Author(s).
URI: https://ir.swu.ac.th/jspui/handle/123456789/13040
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85027989574&doi=10.1186%2fs12906-017-1921-y&partnerID=40&md5=f3c3da47eb0fb4e8367bc3a8fb2d5c92
ISSN: 14726882
Appears in Collections:Scopus 1983-2021

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