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Glabridin induces apoptosis and autophagy through JNK1/2 pathway in human hepatoma cells

Extensive research results support the use of herbal medicine or natural food to augment therapy for various cancers. Studies have associated glabridin with numerous biological activities, such as regulating energy metabolism and estrogenic, neuroprotective, antiosteoporotic, and skin-whitening acti... Full description

Journal Title: Phytomedicine (Stuttgart) 2016-04-15, Vol.23 (4), p.359-366
Main Author: Hsieh, Ming-Ju
Other Authors: Chen, Mu-Kuan , Chen, Chih-Jung , Hsieh, Ming-Chang , Lo, Yu-Sheng , Chuang, Yi-Ching , Chiou, Hui-Ling , Yang, Shun-Fa
Format: Electronic Article Electronic Article
Language: English
Subjects:
JNK
Quelle: Alma/SFX Local Collection
Publisher: Germany: Elsevier GmbH
ID: ISSN: 0944-7113
Link: https://www.ncbi.nlm.nih.gov/pubmed/27002406
Zum Text:
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title: Glabridin induces apoptosis and autophagy through JNK1/2 pathway in human hepatoma cells
format: Article
creator:
  • Hsieh, Ming-Ju
  • Chen, Mu-Kuan
  • Chen, Chih-Jung
  • Hsieh, Ming-Chang
  • Lo, Yu-Sheng
  • Chuang, Yi-Ching
  • Chiou, Hui-Ling
  • Yang, Shun-Fa
subjects:
  • Antineoplastic Agents, Phytogenic - pharmacology
  • Antineoplastic Agents, Phytogenic - therapeutic use
  • Apoptosis
  • Apoptosis - drug effects
  • Apoptosis Regulatory Proteins - metabolism
  • Autophagy
  • Autophagy - drug effects
  • B cells
  • Beclin-1
  • Biological products industry
  • Carcinoma, Hepatocellular - drug therapy
  • Carcinoma, Hepatocellular - metabolism
  • Caspases - metabolism
  • Cell Line, Tumor
  • Cell Proliferation - drug effects
  • Cell Survival - drug effects
  • Glabridin
  • Glycyrrhiza - chemistry
  • Hepatoma
  • Humans
  • Isoflavones - pharmacology
  • Isoflavones - therapeutic use
  • JNK
  • Liver cancer
  • Liver Neoplasms - drug therapy
  • Liver Neoplasms - metabolism
  • MAP Kinase Signaling System
  • Membrane Proteins - metabolism
  • p38 Mitogen-Activated Protein Kinases - metabolism
  • Phenols - pharmacology
  • Phenols - therapeutic use
  • Physiological aspects
  • Phytotherapy
  • Plant Extracts - pharmacology
  • Plant Extracts - therapeutic use
  • Signal Transduction - drug effects
ispartof: Phytomedicine (Stuttgart), 2016-04-15, Vol.23 (4), p.359-366
description: Extensive research results support the use of herbal medicine or natural food to augment therapy for various cancers. Studies have associated glabridin with numerous biological activities, such as regulating energy metabolism and estrogenic, neuroprotective, antiosteoporotic, and skin-whitening activities. However, how glabridin affects tumor cell autophagy has not been clearly determined. Autophagy is a lysosomal degradation pathway essential for cell survival and tissue homeostasis. In this study, the roles of autophagy and related signaling pathways during glabridin-induced autophagy in human liver cancer cells were investigated. Additionally, the molecular mechanism of the anticancer effects of glabridin in human hepatoma cells was investigated. The results revealed that glabridin significantly inhibited cell proliferation in human hepatoma cells. Glabridin induced apoptosis dose-dependently in Huh7 cells through caspase-3, -8, and -9 activation and PARP cleavage. Furthermore, autophagy was detected as early as 12h after exposure to a low dose of glabridin, as indicated by the up-regulated expression of LC3-II and beclin-1 proteins. The inhibition of JNK1/2 and p38 MAPK by specific inhibitors significantly reduced glabridin-induced activation of caspases-3, -8, and -9. Blocking autophagy sensitize the Huh7 cells to apoptosis. This study demonstrated for the first time that autophagy occurs earlier than apoptosis does during glabridin-induced apoptosis in human liver cancer cell lines. Glabridin induces Huh7 cell death through apoptosis through the p38 MAPK and JNK1/2 pathways and is a potential chemopreventive agent against human hepatoma. [Display omitted]
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0944-7113
fulltext: fulltext
issn:
  • 0944-7113
  • 1618-095X
url: Link


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titleGlabridin induces apoptosis and autophagy through JNK1/2 pathway in human hepatoma cells
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creatorHsieh, Ming-Ju ; Chen, Mu-Kuan ; Chen, Chih-Jung ; Hsieh, Ming-Chang ; Lo, Yu-Sheng ; Chuang, Yi-Ching ; Chiou, Hui-Ling ; Yang, Shun-Fa
creatorcontribHsieh, Ming-Ju ; Chen, Mu-Kuan ; Chen, Chih-Jung ; Hsieh, Ming-Chang ; Lo, Yu-Sheng ; Chuang, Yi-Ching ; Chiou, Hui-Ling ; Yang, Shun-Fa
descriptionExtensive research results support the use of herbal medicine or natural food to augment therapy for various cancers. Studies have associated glabridin with numerous biological activities, such as regulating energy metabolism and estrogenic, neuroprotective, antiosteoporotic, and skin-whitening activities. However, how glabridin affects tumor cell autophagy has not been clearly determined. Autophagy is a lysosomal degradation pathway essential for cell survival and tissue homeostasis. In this study, the roles of autophagy and related signaling pathways during glabridin-induced autophagy in human liver cancer cells were investigated. Additionally, the molecular mechanism of the anticancer effects of glabridin in human hepatoma cells was investigated. The results revealed that glabridin significantly inhibited cell proliferation in human hepatoma cells. Glabridin induced apoptosis dose-dependently in Huh7 cells through caspase-3, -8, and -9 activation and PARP cleavage. Furthermore, autophagy was detected as early as 12h after exposure to a low dose of glabridin, as indicated by the up-regulated expression of LC3-II and beclin-1 proteins. The inhibition of JNK1/2 and p38 MAPK by specific inhibitors significantly reduced glabridin-induced activation of caspases-3, -8, and -9. Blocking autophagy sensitize the Huh7 cells to apoptosis. This study demonstrated for the first time that autophagy occurs earlier than apoptosis does during glabridin-induced apoptosis in human liver cancer cell lines. Glabridin induces Huh7 cell death through apoptosis through the p38 MAPK and JNK1/2 pathways and is a potential chemopreventive agent against human hepatoma. [Display omitted]
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languageeng
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subjectAntineoplastic Agents, Phytogenic - pharmacology ; Antineoplastic Agents, Phytogenic - therapeutic use ; Apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - metabolism ; Autophagy ; Autophagy - drug effects ; B cells ; Beclin-1 ; Biological products industry ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - metabolism ; Caspases - metabolism ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Glabridin ; Glycyrrhiza - chemistry ; Hepatoma ; Humans ; Isoflavones - pharmacology ; Isoflavones - therapeutic use ; JNK ; Liver cancer ; Liver Neoplasms - drug therapy ; Liver Neoplasms - metabolism ; MAP Kinase Signaling System ; Membrane Proteins - metabolism ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phenols - pharmacology ; Phenols - therapeutic use ; Physiological aspects ; Phytotherapy ; Plant Extracts - pharmacology ; Plant Extracts - therapeutic use ; Signal Transduction - drug effects
ispartofPhytomedicine (Stuttgart), 2016-04-15, Vol.23 (4), p.359-366
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descriptionExtensive research results support the use of herbal medicine or natural food to augment therapy for various cancers. Studies have associated glabridin with numerous biological activities, such as regulating energy metabolism and estrogenic, neuroprotective, antiosteoporotic, and skin-whitening activities. However, how glabridin affects tumor cell autophagy has not been clearly determined. Autophagy is a lysosomal degradation pathway essential for cell survival and tissue homeostasis. In this study, the roles of autophagy and related signaling pathways during glabridin-induced autophagy in human liver cancer cells were investigated. Additionally, the molecular mechanism of the anticancer effects of glabridin in human hepatoma cells was investigated. The results revealed that glabridin significantly inhibited cell proliferation in human hepatoma cells. Glabridin induced apoptosis dose-dependently in Huh7 cells through caspase-3, -8, and -9 activation and PARP cleavage. Furthermore, autophagy was detected as early as 12h after exposure to a low dose of glabridin, as indicated by the up-regulated expression of LC3-II and beclin-1 proteins. The inhibition of JNK1/2 and p38 MAPK by specific inhibitors significantly reduced glabridin-induced activation of caspases-3, -8, and -9. Blocking autophagy sensitize the Huh7 cells to apoptosis. This study demonstrated for the first time that autophagy occurs earlier than apoptosis does during glabridin-induced apoptosis in human liver cancer cell lines. Glabridin induces Huh7 cell death through apoptosis through the p38 MAPK and JNK1/2 pathways and is a potential chemopreventive agent against human hepatoma. [Display omitted]
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2Apoptosis
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4Apoptosis Regulatory Proteins - metabolism
5Autophagy
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9Biological products industry
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11Carcinoma, Hepatocellular - metabolism
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13Cell Line, Tumor
14Cell Proliferation - drug effects
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25Liver Neoplasms - metabolism
26MAP Kinase Signaling System
27Membrane Proteins - metabolism
28p38 Mitogen-Activated Protein Kinases - metabolism
29Phenols - pharmacology
30Phenols - therapeutic use
31Physiological aspects
32Phytotherapy
33Plant Extracts - pharmacology
34Plant Extracts - therapeutic use
35Signal Transduction - drug effects
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abstractExtensive research results support the use of herbal medicine or natural food to augment therapy for various cancers. Studies have associated glabridin with numerous biological activities, such as regulating energy metabolism and estrogenic, neuroprotective, antiosteoporotic, and skin-whitening activities. However, how glabridin affects tumor cell autophagy has not been clearly determined. Autophagy is a lysosomal degradation pathway essential for cell survival and tissue homeostasis. In this study, the roles of autophagy and related signaling pathways during glabridin-induced autophagy in human liver cancer cells were investigated. Additionally, the molecular mechanism of the anticancer effects of glabridin in human hepatoma cells was investigated. The results revealed that glabridin significantly inhibited cell proliferation in human hepatoma cells. Glabridin induced apoptosis dose-dependently in Huh7 cells through caspase-3, -8, and -9 activation and PARP cleavage. Furthermore, autophagy was detected as early as 12h after exposure to a low dose of glabridin, as indicated by the up-regulated expression of LC3-II and beclin-1 proteins. The inhibition of JNK1/2 and p38 MAPK by specific inhibitors significantly reduced glabridin-induced activation of caspases-3, -8, and -9. Blocking autophagy sensitize the Huh7 cells to apoptosis. This study demonstrated for the first time that autophagy occurs earlier than apoptosis does during glabridin-induced apoptosis in human liver cancer cell lines. Glabridin induces Huh7 cell death through apoptosis through the p38 MAPK and JNK1/2 pathways and is a potential chemopreventive agent against human hepatoma. [Display omitted]
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