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Targeting epigenetics and Nrf2-pathway by dietary phytochemicals
Descriptive
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Title
Targeting epigenetics and Nrf2-pathway by dietary phytochemicals
SubTitle
promising cancer prevention approach
Name
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Yang
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Yuqing
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Yuqing Yang
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author
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Kong
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Ah-Ng Tony
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Ah-Ng Tony Kong
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Advisory Committee
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chair
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Chen
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Suzie
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Suzie Chen
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Advisory Committee
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internal member
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(type = family)
Kagan
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(type = given)
Leonid Kagan
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Leonid Kagan Kagan
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Advisory Committee
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internal member
Name
(type = personal)
NamePart
(type = family)
Cai
NamePart
(type = given)
Li
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Li Cai
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Advisory Committee
Role
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(authority = RULIB)
outside member
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Rutgers University
Role
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(authority = RULIB)
degree grantor
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School of Graduate Studies
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school
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Text
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theses
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2017
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2017-10
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2017
Place
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xx
Language
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eng
Abstract
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The induction of nuclear factor (erythroid-derived 2)-like 2 (Nrf2)- antioxidant response elements (ARE)-mediated antioxidant enzymes provides a cellular defense against oxidative stress, a major drive of human diseases such as the tumor. Phytochemicals in folk medicine are widely being used as natural sources to develop novel therapeutics. Astaxanthin (AST) with potent antioxidant activity in combination with omega-3 fatty acid docosahexaenoic acid (DHA) or eicosapentaenoic acid (EPA) at low concentration showed synergistic defense against oxidative stress via Nrf2-ARE pathway. The three natural chemicals alone and in combination elevated cellular GSH level, increased total antioxidant activity, induced mRNA expression of Nrf2 and its downstream genes in human HepG2-C8 cells. In addition, AST significantly decreased the methylation of GSTP1 promoter region and restored the expression of GSTP1, which is involved in detoxification and metabolism to prevent genome damage and cancer initiation. It suggests a correlation between the DNA methylation and GSTP1 expression in human prostate LNCaP cells. AST reduced protein expression and enzyme activity of the DNA methyltransferases (DNMTs). Moreover, we demonstrated that Nrf2 shows protective role in epidermis against inflammation and extracellular matrix (ECM) damage induced by the UVB-irradiation. As compared with the wildt-ype (WT) mice, Nrf2 knockout (KO) mice showed the increased protein expression of inflammatory markers, including P53, macrophage inflammatory protein-2 (MIP-2), and pro-matrix metalloproteinase-9 (pro-MMP-9). The protective effects of Nrf2 in response to the UVB-irradiation were mediated by increased HO-1 protein expression. Moreover, we conducted genome-wide analysis of DNA methylation in UVB- and DMBA-TPA induced mouse skin tumor models to identify genes and pathways with significant changes. The top-ranked genes and pathways will provide insight into the discovery of key genes in skin tumor initiation and progression so as to provide potential preventive biomarkers. Furthermore, we demonstrated that ursolic acid (UA), and sulforaphane (SFN) reduced in vivo skin carcinogenesis induced by UVB-irradiation. In conclusion, dietary natural chemicals alone or in combination attenuate oxidative stress, inflammation and even carcinogenesis through modulation of genetic and epigenetic events, and provide promising insights into cancer prevention.
Subject
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Topic
Pharmaceutical Science
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Title
Rutgers University Electronic Theses and Dissertations
Identifier
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ETD_8348
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electronic resource
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application/pdf
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Extent
1 online resource (xviii, 210 p. : ill.)
Note
(type = degree)
Ph.D.
Note
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Includes bibliographical references
Subject
(authority = ETD-LCSH)
Topic
Epigenetics
Note
(type = statement of responsibility)
by Yuqing Yang
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Title
School of Graduate Studies Electronic Theses and Dissertations
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rucore10001600001
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NjNbRU
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doi:10.7282/T3K64N8D
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ETD doctoral
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Rights
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The author owns the copyright to this work.
RightsHolder
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Name
FamilyName
Yang
GivenName
Yuqing
Role
Copyright Holder
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Permission or license
DateTime
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2017-09-13 15:41:52
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Name
Yuqing Yang
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Affiliation
Rutgers University. School of Graduate Studies
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Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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2017-10-31
DateTime
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2019-10-31
Type
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Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 31st, 2019.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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