PMID- 36614036
OWN - NLM
STAT- MEDLINE
DCOM- 20230112
LR  - 20230112
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 24
IP  - 1
DP  - 2022 Dec 29
TI  - NRF2 in Cancer: Cross-Talk with Oncogenic Pathways and Involvement in 
      Gammaherpesvirus-Driven Carcinogenesis.
LID - 10.3390/ijms24010595 [doi]
LID - 595
AB  - Expanding knowledge of the molecular mechanisms at the basis of tumor 
      development, especially the cross-talk between oncogenic pathways, will possibly 
      lead to better tailoring of anticancer therapies. Nuclear factor erythroid 
      2-related factor 2 (NRF2) plays a central role in cancer progression, not only 
      because of its antioxidant activity but also because it establishes cross-talk 
      with several oncogenic pathways, including Heat Shock Factor1 (HSF1), mammalian 
      target of rapamycin (mTOR), and mutant (mut) p53. Moreover, the involvement of 
      NRF2 in gammaherpesvirus-driven carcinogenesis is particularly interesting. These 
      viruses indeed hijack the NRF2 pathway to sustain the survival of tumor cells in 
      which they establish a latent infection and to avoid a too-high increase of 
      reactive oxygen species (ROS) when these cancer cells undergo treatments that 
      induce viral replication. Interestingly, NRF2 activation may prevent 
      gammaherpesvirus-driven oncogenic transformation, highlighting how manipulating 
      the NRF2 pathway in the different phases of gammaherpesvirus-mediated 
      carcinogenesis may lead to different outcomes. This review will highlight the 
      mechanistic interplay between NRF2 and some oncogenic pathways and its 
      involvement in gammaherpesviruses biology to recapitulate published evidence 
      useful for potential application in cancer therapy.
FAU - Cirone, Mara
AU  - Cirone M
AUID- ORCID: 0000-0002-2207-9624
AD  - Department of Experimental Medicine, University of Rome La Sapienza, Viale Regina 
      Elena 324, 00161 Rome, Italy.
FAU - D'Orazi, Gabriella
AU  - D'Orazi G
AUID- ORCID: 0000-0001-6876-9105
AD  - Department of Neurosciences, Imaging and Clinical Sciences, University "G. 
      D'Annunzio", 66013 Chieti, Italy.
AD  - School of Medicine, UniCamillus International University, 00131 Rome, Italy.
LA  - eng
GR  - Id.16742/Italian Association for Cancer Research/
GR  - Id.23040/Italian Association for Cancer Research/
PT  - Journal Article
PT  - Review
DEP - 20221229
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (NFE2L2 protein, human)
SB  - IM
MH  - Humans
MH  - Autophagy
MH  - Carcinogenesis/genetics/metabolism
MH  - Cell Transformation, Neoplastic/genetics/metabolism
MH  - *Neoplasms/genetics/virology
MH  - *NF-E2-Related Factor 2/genetics/metabolism
MH  - Oxidative Stress/physiology
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/physiology
MH  - *Gammaherpesvirinae
PMC - PMC9820659
OTO - NOTNLM
OT  - KEAP1
OT  - NFkB
OT  - NRF2
OT  - STAT3
OT  - apoptosis
OT  - autophagy
OT  - cancer therapy
OT  - chemoresistance
OT  - gammaherpesviruses
OT  - inflammation
OT  - mTOR
OT  - oxidative stress
OT  - p21
OT  - p53
OT  - p62/SQSTM1
OT  - reactive oxygen species (ROS)
COIS- The authors declare no conflict of interest.
EDAT- 2023/01/09 06:00
MHDA- 2023/01/11 06:00
PMCR- 2022/12/29
CRDT- 2023/01/08 01:24
PHST- 2022/11/11 00:00 [received]
PHST- 2022/12/26 00:00 [revised]
PHST- 2022/12/27 00:00 [accepted]
PHST- 2023/01/08 01:24 [entrez]
PHST- 2023/01/09 06:00 [pubmed]
PHST- 2023/01/11 06:00 [medline]
PHST- 2022/12/29 00:00 [pmc-release]
AID - ijms24010595 [pii]
AID - ijms-24-00595 [pii]
AID - 10.3390/ijms24010595 [doi]
PST - epublish
SO  - Int J Mol Sci. 2022 Dec 29;24(1):595. doi: 10.3390/ijms24010595.