PMID- 31052524
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 2072-6694 (Print)
IS  - 2072-6694 (Electronic)
IS  - 2072-6694 (Linking)
VI  - 11
IP  - 5
DP  - 2019 May 2
TI  - Mutant p53 and Cellular Stress Pathways: A Criminal Alliance That Promotes Cancer 
      Progression.
LID - 10.3390/cancers11050614 [doi]
LID - 614
AB  - The capability of cancer cells to manage stress induced by hypoxia, nutrient 
      shortage, acidosis, redox imbalance, loss of calcium homeostasis and exposure to 
      drugs is a key factor to ensure cancer survival and chemoresistance. Among the 
      protective mechanisms utilized by cancer cells to cope with stress a pivotal role 
      is played by the activation of heat shock proteins (HSP) response, anti-oxidant 
      response induced by nuclear factor erythroid 2-related factor 2 (NRF2), the 
      hypoxia-inducible factor-1 (HIF-1), the unfolded protein response (UPR) and 
      autophagy, cellular processes strictly interconnected. However, depending on the 
      type, intensity or duration of cellular stress, the balance between pro-survival 
      and pro-death pathways may change, and cell survival may be shifted into cell 
      death. Mutations of p53 (mutp53), occurring in more than 50% of human cancers, 
      may confer oncogenic gain-of-function (GOF) to the protein, mainly due to its 
      stabilization and interaction with the above reported cellular pathways that help 
      cancer cells to adapt to stress. This review will focus on the interplay of 
      mutp53 with HSPs, NRF2, UPR, and autophagy and discuss how the manipulation of 
      these interconnected processes may tip the balance towards cell death or 
      survival, particularly in response to therapies.
FAU - D'Orazi, Gabriella
AU  - D'Orazi G
AUID- ORCID: 0000-0001-6876-9105
AD  - Department of Medical Sciences, University 'G. d'Annunzio', 66013 Chieti, Italy. 
      gdorazi@unich.it.
AD  - Department of Research, IRCCS Regina Elena National Cancer Institute, 00144 Rome, 
      Italy. gdorazi@unich.it.
FAU - Cirone, Mara
AU  - Cirone M
AUID- ORCID: 0000-0002-2207-9624
AD  - Department of Experimental Medicine, "Sapienza" University of Rome, 00185 Rome, 
      Italy. mara.cirone@uniroma1.it.
AD  - Laboratory Affiliated to Pasteur Institute, Italy-Foundation Cenci Bolognetti, 
      00161 Rome, Italy. mara.cirone@uniroma1.it.
LA  - eng
GR  - IG11377, IG16742/Associazione Italiana per la Ricerca sul Cancro/
GR  - 2018/Fondi Ateneo ex 60%,University "G. d'Annunzio"/
GR  - 2014-033-R.O./ASI (Agenzia Spaziale Italiana)/
GR  - 2018/Pasteur Insitute-Italia Fondazione Cenci-Bolognett/
GR  - N degrees  C26A15CX3M/Fondi Ateneo, University Sapienza, Ricerche Universitarie/
PT  - Journal Article
PT  - Review
DEP - 20190502
PL  - Switzerland
TA  - Cancers (Basel)
JT  - Cancers
JID - 101526829
PMC - PMC6563084
OTO - NOTNLM
OT  - anticancer therapy
OT  - antioxidant response
OT  - autophagy
OT  - endoplasmic reticulum (ER) stress
OT  - gain-of-function (GOF)
OT  - heat shock protein (HSP)
OT  - hypoxia-inducible factor 1 (HIF-1)
OT  - mutant p53 (mutp53)
OT  - nuclear factor erythroid 2-related factor 2 (NRF2)
OT  - unfolded protein response (UPR)
COIS- The authors declare no conflict of interest.
EDAT- 2019/05/06 06:00
MHDA- 2019/05/06 06:01
PMCR- 2019/05/02
CRDT- 2019/05/05 06:00
PHST- 2019/04/16 00:00 [received]
PHST- 2019/04/27 00:00 [revised]
PHST- 2019/05/01 00:00 [accepted]
PHST- 2019/05/05 06:00 [entrez]
PHST- 2019/05/06 06:00 [pubmed]
PHST- 2019/05/06 06:01 [medline]
PHST- 2019/05/02 00:00 [pmc-release]
AID - cancers11050614 [pii]
AID - cancers-11-00614 [pii]
AID - 10.3390/cancers11050614 [doi]
PST - epublish
SO  - Cancers (Basel). 2019 May 2;11(5):614. doi: 10.3390/cancers11050614.