PMID- 36335520
OWN - NLM
STAT- MEDLINE
DCOM- 20230131
LR  - 20230202
IS  - 1573-4978 (Electronic)
IS  - 0301-4851 (Linking)
VI  - 50
IP  - 1
DP  - 2023 Jan
TI  - NRF2 modulation in TRAMP mice: an in vivo model of prostate cancer.
PG  - 873-881
LID - 10.1007/s11033-022-08052-2 [doi]
AB  - BACKGROUND: Prostate cancer (PCa) is one of the most common cancers worldwide and 
      oxidative stress is involved in its occurrence, development and progression. In 
      fact, in transgenic adenocarcinoma of mouse prostate (TRAMP) mice, prostate 
      cancer onset is associated with the methylation of the first five CpG in the 
      nuclear factor erythroid 2-related factor 2 (NRF2) promoter, a key regulator of 
      oxidative stress response, leading to its downregulation and accumulation of 
      reactive oxygen species (ROS). It has been demonstrated that both natural and 
      synthetic compounds can reactivate NRF2 expression inhibiting the methylation 
      status of its promoter by downregulation of DNA methyltransferases (DNMTs) and 
      histone deacetylases (HDACs). Interestingly, NRF2 re-expression significantly 
      reduced prostate cancer onset in TRAMP mice highlighting an important role of 
      NRF2 in prostate tumorigenesis. METHODS AND RESULTS: We analysed the current 
      literature regarding the role of natural and synthetic compounds in modulating 
      NRF2 pathway in TRAMP mice, an in vivo model of prostate cancer, to give an 
      overview on prostate carcinogenesis and its possible prevention. CONCLUSION: We 
      can conclude that specific natural and synthetic compounds can downregulate DNMTs 
      and/or HDACs inhibiting the methylation status of NRF2 promoter, then 
      reactivating the expression of NRF2 protecting normal prostatic cells from ROS 
      damage and tumorigenesis.
CI  - (c) 2022. The Author(s), under exclusive licence to Springer Nature B.V.
FAU - Marzioni, Daniela
AU  - Marzioni D
AD  - Department of Experimental and Clinical Medicine, Universita Politecnica Delle 
      Marche, 60126, Ancona, Italy.
FAU - Mazzucchelli, Roberta
AU  - Mazzucchelli R
AD  - Department of Biomedical Sciences and Public Health, Section of Pathological 
      Anatomy, School of Medicine, United Hospitals, Universita Politecnica Delle 
      Marche, Ancona, Italy.
FAU - Fantone, Sonia
AU  - Fantone S
AD  - Department of Experimental and Clinical Medicine, Universita Politecnica Delle 
      Marche, 60126, Ancona, Italy.
FAU - Tossetta, Giovanni
AU  - Tossetta G
AUID- ORCID: 0000-0001-7003-1230
AD  - Department of Experimental and Clinical Medicine, Universita Politecnica Delle 
      Marche, 60126, Ancona, Italy. g.tossetta@univpm.it.
AD  - Clinic of Obstetrics and Gynaecology, Department of Clinical Sciences, Universita 
      Politecnica Delle Marche, Salesi Hospital, Azienda Ospedaliero Universitaria, 
      Ancona, Italy. g.tossetta@univpm.it.
LA  - eng
GR  - SG-2018-12367994/Ministero della Salute/
PT  - Journal Article
PT  - Review
DEP - 20221106
PL  - Netherlands
TA  - Mol Biol Rep
JT  - Molecular biology reports
JID - 0403234
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Male
MH  - Humans
MH  - Mice
MH  - Animals
MH  - Mice, Transgenic
MH  - *NF-E2-Related Factor 2/genetics/metabolism
MH  - Epigenesis, Genetic
MH  - Reactive Oxygen Species/metabolism
MH  - *Prostatic Neoplasms/metabolism
MH  - DNA Methylation/genetics
MH  - Carcinogenesis/genetics
OTO - NOTNLM
OT  - Carcinogenesis
OT  - Compounds
OT  - NRF2
OT  - Prostate cancer
OT  - Signaling
OT  - TRAMP mice
EDAT- 2022/11/07 06:00
MHDA- 2023/02/01 06:00
CRDT- 2022/11/06 14:00
PHST- 2022/08/27 00:00 [received]
PHST- 2022/10/19 00:00 [accepted]
PHST- 2022/11/07 06:00 [pubmed]
PHST- 2023/02/01 06:00 [medline]
PHST- 2022/11/06 14:00 [entrez]
AID - 10.1007/s11033-022-08052-2 [pii]
AID - 10.1007/s11033-022-08052-2 [doi]
PST - ppublish
SO  - Mol Biol Rep. 2023 Jan;50(1):873-881. doi: 10.1007/s11033-022-08052-2. Epub 2022 
      Nov 6.