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Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate

PURPOSE: Our previous experiments show that the main constituent of green-tea catechins, (−)-epigallocatechin gallate (EGCG), completely prevents tumor promotion on mouse skin initiated with 7,12-dimethylbenz(a)anthracene followed by okadaic acid and that EGCG and green tea extract prevent cancer de...

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Autores principales: Fujiki, Hirota, Sueoka, Eisaburo, Rawangkan, Anchalee, Suganuma, Masami
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5693978/
https://www.ncbi.nlm.nih.gov/pubmed/28942499
http://dx.doi.org/10.1007/s00432-017-2515-2
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author Fujiki, Hirota
Sueoka, Eisaburo
Rawangkan, Anchalee
Suganuma, Masami
author_facet Fujiki, Hirota
Sueoka, Eisaburo
Rawangkan, Anchalee
Suganuma, Masami
author_sort Fujiki, Hirota
collection PubMed
description PURPOSE: Our previous experiments show that the main constituent of green-tea catechins, (−)-epigallocatechin gallate (EGCG), completely prevents tumor promotion on mouse skin initiated with 7,12-dimethylbenz(a)anthracene followed by okadaic acid and that EGCG and green tea extract prevent cancer development in a wide range of target organs in rodents. Therefore, we focused our attention on human cancer stem cells (CSCs) as targets of cancer prevention and treatment with EGCG. METHODS: The numerous reports concerning anticancer activity of EGCG against human CSCs enriched from cancer cell lines were gathered from a search of PubMed, and we hope our review of the literatures will provide a broad selection for the effects of EGCG on various human CSCs. RESULTS: Based on our theoretical study, we discuss the findings as follows: (1) Compared with the parental cells, human CSCs express increased levels of the stemness markers Nanog, Oct4, Sox2, CD44, CD133, as well as the EMT markers, Twist, Snail, vimentin, and also aldehyde dehydrogenase. They showed decreased levels of E-cadherin and cyclin D1. (2) EGCG inhibits the transcription and translation of genes encoding stemness markers, indicating that EGCG generally inhibits the self-renewal of CSCs. (3) EGCG inhibits the expression of the epithelial-mesenchymal transition phenotypes of human CSCs. (4) The inhibition of EGCG of the stemness of CSCs was weaker compared with parental cells. (5) The weak inhibitory activity of EGCG increased synergistically in combination with anticancer drugs. CONCLUSIONS: Green tea prevents human cancer, and the combination of EGCG and anticancer drugs confers cancer treatment with tissue-agnostic efficacy.
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spelling pubmed-56939782017-11-30 Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate Fujiki, Hirota Sueoka, Eisaburo Rawangkan, Anchalee Suganuma, Masami J Cancer Res Clin Oncol Review – Cancer Research PURPOSE: Our previous experiments show that the main constituent of green-tea catechins, (−)-epigallocatechin gallate (EGCG), completely prevents tumor promotion on mouse skin initiated with 7,12-dimethylbenz(a)anthracene followed by okadaic acid and that EGCG and green tea extract prevent cancer development in a wide range of target organs in rodents. Therefore, we focused our attention on human cancer stem cells (CSCs) as targets of cancer prevention and treatment with EGCG. METHODS: The numerous reports concerning anticancer activity of EGCG against human CSCs enriched from cancer cell lines were gathered from a search of PubMed, and we hope our review of the literatures will provide a broad selection for the effects of EGCG on various human CSCs. RESULTS: Based on our theoretical study, we discuss the findings as follows: (1) Compared with the parental cells, human CSCs express increased levels of the stemness markers Nanog, Oct4, Sox2, CD44, CD133, as well as the EMT markers, Twist, Snail, vimentin, and also aldehyde dehydrogenase. They showed decreased levels of E-cadherin and cyclin D1. (2) EGCG inhibits the transcription and translation of genes encoding stemness markers, indicating that EGCG generally inhibits the self-renewal of CSCs. (3) EGCG inhibits the expression of the epithelial-mesenchymal transition phenotypes of human CSCs. (4) The inhibition of EGCG of the stemness of CSCs was weaker compared with parental cells. (5) The weak inhibitory activity of EGCG increased synergistically in combination with anticancer drugs. CONCLUSIONS: Green tea prevents human cancer, and the combination of EGCG and anticancer drugs confers cancer treatment with tissue-agnostic efficacy. Springer Berlin Heidelberg 2017-09-23 2017 /pmc/articles/PMC5693978/ /pubmed/28942499 http://dx.doi.org/10.1007/s00432-017-2515-2 Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review – Cancer Research
Fujiki, Hirota
Sueoka, Eisaburo
Rawangkan, Anchalee
Suganuma, Masami
Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
title Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
title_full Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
title_fullStr Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
title_full_unstemmed Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
title_short Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
title_sort human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
topic Review – Cancer Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5693978/
https://www.ncbi.nlm.nih.gov/pubmed/28942499
http://dx.doi.org/10.1007/s00432-017-2515-2
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