PMID- 34845361
OWN - NLM
STAT- MEDLINE
DCOM- 20220428
LR  - 20221130
IS  - 1532-1827 (Electronic)
IS  - 0007-0920 (Print)
IS  - 0007-0920 (Linking)
VI  - 126
IP  - 9
DP  - 2022 May
TI  - Genetic and epigenetic regulation of the NRF2-KEAP1 pathway in human lung cancer.
PG  - 1244-1252
LID - 10.1038/s41416-021-01642-0 [doi]
AB  - Electrophilic and oxidative stress is caused when homeostatic mechanisms are 
      disrupted. A major defense mechanism involves the activation of the nuclear 
      factor erythroid 2-related factor 2 (NRF2) transcription factor encoded by the 
      NFE2L2 gene, which can accelerate the detoxification of electrophilic carcinogens 
      and prevent cancer and on the other hand in certain exposure contexts may 
      exacerbate the carcinogenic process. NRF2-target genes activated under these 
      conditions can be used as biomarkers of stress signalling, while activation of 
      NRF2 can also reveal the epigenetic mechanisms that modulate NFE2L2 expression. 
      Epigenetic mechanisms that regulate NFE2L2 and the gene for its adaptor protein 
      KEAP1 include DNA methylation, histone modifications and microRNA. Understanding 
      the activation of the NRF2-KEAP1 signalling pathway in human lung cancer, its 
      epigenetic regulation and its role in oncogenesis is the subject of this review.
CI  - (c) 2021. The Author(s), under exclusive licence to Springer Nature Limited.
FAU - Camina, Nuria
AU  - Camina N
AUID- ORCID: 0000-0002-0714-7705
AD  - Department of Systems Pharmacology & Translational Therapeutics, Center of 
      Excellence in Environmental Toxicology, Perelman School of Medicine, University 
      of Pennsylvania, Philadelphia, PA, USA.
FAU - Penning, Trevor M
AU  - Penning TM
AUID- ORCID: 0000-0002-3937-1066
AD  - Department of Systems Pharmacology & Translational Therapeutics, Center of 
      Excellence in Environmental Toxicology, Perelman School of Medicine, University 
      of Pennsylvania, Philadelphia, PA, USA. penning@upenn.edu.
LA  - eng
GR  - P30 ES013508/ES/NIEHS NIH HHS/United States
GR  - R01 ES029294/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20211129
PL  - England
TA  - Br J Cancer
JT  - British journal of cancer
JID - 0370635
RN  - 0 (KEAP1 protein, human)
RN  - 0 (Kelch-Like ECH-Associated Protein 1)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NFE2L2 protein, human)
SB  - IM
MH  - DNA Methylation
MH  - *Epigenesis, Genetic
MH  - Humans
MH  - *Kelch-Like ECH-Associated Protein 1/genetics/metabolism
MH  - *Lung Neoplasms/genetics
MH  - *NF-E2-Related Factor 2/genetics/metabolism
MH  - Oxidative Stress/genetics
PMC - PMC9042933
COIS- The authors declare no conflict of interest.
EDAT- 2021/12/01 06:00
MHDA- 2022/04/29 06:00
PMCR- 2022/11/29
CRDT- 2021/11/30 06:49
PHST- 2021/03/02 00:00 [received]
PHST- 2021/11/12 00:00 [accepted]
PHST- 2021/10/23 00:00 [revised]
PHST- 2021/12/01 06:00 [pubmed]
PHST- 2022/04/29 06:00 [medline]
PHST- 2021/11/30 06:49 [entrez]
PHST- 2022/11/29 00:00 [pmc-release]
AID - 10.1038/s41416-021-01642-0 [pii]
AID - 1642 [pii]
AID - 10.1038/s41416-021-01642-0 [doi]
PST - ppublish
SO  - Br J Cancer. 2022 May;126(9):1244-1252. doi: 10.1038/s41416-021-01642-0. Epub 
      2021 Nov 29.