The p53 family member p73 in the regulation of cell stress response
Abstract During oncogenesis, cells become unrestrictedly proliferative thereby altering the tissue homeostasis and resulting in subsequent hyperplasia. This process is paralleled by resumption of cell cycle, aberrant DNA repair and blunting the apoptotic program in response to DNA damage. In most hu...
Guardado en:
| Autores principales: | , , , , , , , , , , , , , |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
BMC
2021
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/c363e2f06edb43798b66b01caeff273a |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| id |
oai:doaj.org-article:c363e2f06edb43798b66b01caeff273a |
|---|---|
| record_format |
dspace |
| spelling |
oai:doaj.org-article:c363e2f06edb43798b66b01caeff273a2021-11-14T12:08:42ZThe p53 family member p73 in the regulation of cell stress response10.1186/s13062-021-00307-51745-6150https://doaj.org/article/c363e2f06edb43798b66b01caeff273a2021-11-01T00:00:00Zhttps://doi.org/10.1186/s13062-021-00307-5https://doaj.org/toc/1745-6150Abstract During oncogenesis, cells become unrestrictedly proliferative thereby altering the tissue homeostasis and resulting in subsequent hyperplasia. This process is paralleled by resumption of cell cycle, aberrant DNA repair and blunting the apoptotic program in response to DNA damage. In most human cancers these processes are associated with malfunctioning of tumor suppressor p53. Intriguingly, in some cases two other members of the p53 family of proteins, transcription factors p63 and p73, can compensate for loss of p53. Although both p63 and p73 can bind the same DNA sequences as p53 and their transcriptionally active isoforms are able to regulate the expression of p53-dependent genes, the strongest overlap with p53 functions was detected for p73. Surprisingly, unlike p53, the p73 is rarely lost or mutated in cancers. On the contrary, its inactive isoforms are often overexpressed in cancer. In this review, we discuss several lines of evidence that cancer cells develop various mechanisms to repress p73-mediated cell death. Moreover, p73 isoforms may promote cancer growth by enhancing an anti-oxidative response, the Warburg effect and by repressing senescence. Thus, we speculate that the role of p73 in tumorigenesis can be ambivalent and hence, requires new therapeutic strategies that would specifically repress the oncogenic functions of p73, while keeping its tumor suppressive properties intact.Julian M. RozenbergSvetlana ZverevaAleksandra DalinaIgor BlatovIlya ZubarevDaniil LuppovAlexander BessmertnyiAlexander RomanishinLamak AlsoulaimanVadim KumeikoAlexander KaganskyGerry MelinoCarlo GaniniNikolai A. BarlevBMCarticleCancer hallmarksTumor suppressor p53p73Biology (General)QH301-705.5ENBiology Direct, Vol 16, Iss 1, Pp 1-21 (2021) |
| institution |
DOAJ |
| collection |
DOAJ |
| language |
EN |
| topic |
Cancer hallmarks Tumor suppressor p53 p73 Biology (General) QH301-705.5 |
| spellingShingle |
Cancer hallmarks Tumor suppressor p53 p73 Biology (General) QH301-705.5 Julian M. Rozenberg Svetlana Zvereva Aleksandra Dalina Igor Blatov Ilya Zubarev Daniil Luppov Alexander Bessmertnyi Alexander Romanishin Lamak Alsoulaiman Vadim Kumeiko Alexander Kagansky Gerry Melino Carlo Ganini Nikolai A. Barlev The p53 family member p73 in the regulation of cell stress response |
| description |
Abstract During oncogenesis, cells become unrestrictedly proliferative thereby altering the tissue homeostasis and resulting in subsequent hyperplasia. This process is paralleled by resumption of cell cycle, aberrant DNA repair and blunting the apoptotic program in response to DNA damage. In most human cancers these processes are associated with malfunctioning of tumor suppressor p53. Intriguingly, in some cases two other members of the p53 family of proteins, transcription factors p63 and p73, can compensate for loss of p53. Although both p63 and p73 can bind the same DNA sequences as p53 and their transcriptionally active isoforms are able to regulate the expression of p53-dependent genes, the strongest overlap with p53 functions was detected for p73. Surprisingly, unlike p53, the p73 is rarely lost or mutated in cancers. On the contrary, its inactive isoforms are often overexpressed in cancer. In this review, we discuss several lines of evidence that cancer cells develop various mechanisms to repress p73-mediated cell death. Moreover, p73 isoforms may promote cancer growth by enhancing an anti-oxidative response, the Warburg effect and by repressing senescence. Thus, we speculate that the role of p73 in tumorigenesis can be ambivalent and hence, requires new therapeutic strategies that would specifically repress the oncogenic functions of p73, while keeping its tumor suppressive properties intact. |
| format |
article |
| author |
Julian M. Rozenberg Svetlana Zvereva Aleksandra Dalina Igor Blatov Ilya Zubarev Daniil Luppov Alexander Bessmertnyi Alexander Romanishin Lamak Alsoulaiman Vadim Kumeiko Alexander Kagansky Gerry Melino Carlo Ganini Nikolai A. Barlev |
| author_facet |
Julian M. Rozenberg Svetlana Zvereva Aleksandra Dalina Igor Blatov Ilya Zubarev Daniil Luppov Alexander Bessmertnyi Alexander Romanishin Lamak Alsoulaiman Vadim Kumeiko Alexander Kagansky Gerry Melino Carlo Ganini Nikolai A. Barlev |
| author_sort |
Julian M. Rozenberg |
| title |
The p53 family member p73 in the regulation of cell stress response |
| title_short |
The p53 family member p73 in the regulation of cell stress response |
| title_full |
The p53 family member p73 in the regulation of cell stress response |
| title_fullStr |
The p53 family member p73 in the regulation of cell stress response |
| title_full_unstemmed |
The p53 family member p73 in the regulation of cell stress response |
| title_sort |
p53 family member p73 in the regulation of cell stress response |
| publisher |
BMC |
| publishDate |
2021 |
| url |
https://doaj.org/article/c363e2f06edb43798b66b01caeff273a |
| work_keys_str_mv |
AT julianmrozenberg thep53familymemberp73intheregulationofcellstressresponse AT svetlanazvereva thep53familymemberp73intheregulationofcellstressresponse AT aleksandradalina thep53familymemberp73intheregulationofcellstressresponse AT igorblatov thep53familymemberp73intheregulationofcellstressresponse AT ilyazubarev thep53familymemberp73intheregulationofcellstressresponse AT daniilluppov thep53familymemberp73intheregulationofcellstressresponse AT alexanderbessmertnyi thep53familymemberp73intheregulationofcellstressresponse AT alexanderromanishin thep53familymemberp73intheregulationofcellstressresponse AT lamakalsoulaiman thep53familymemberp73intheregulationofcellstressresponse AT vadimkumeiko thep53familymemberp73intheregulationofcellstressresponse AT alexanderkagansky thep53familymemberp73intheregulationofcellstressresponse AT gerrymelino thep53familymemberp73intheregulationofcellstressresponse AT carloganini thep53familymemberp73intheregulationofcellstressresponse AT nikolaiabarlev thep53familymemberp73intheregulationofcellstressresponse AT julianmrozenberg p53familymemberp73intheregulationofcellstressresponse AT svetlanazvereva p53familymemberp73intheregulationofcellstressresponse AT aleksandradalina p53familymemberp73intheregulationofcellstressresponse AT igorblatov p53familymemberp73intheregulationofcellstressresponse AT ilyazubarev p53familymemberp73intheregulationofcellstressresponse AT daniilluppov p53familymemberp73intheregulationofcellstressresponse AT alexanderbessmertnyi p53familymemberp73intheregulationofcellstressresponse AT alexanderromanishin p53familymemberp73intheregulationofcellstressresponse AT lamakalsoulaiman p53familymemberp73intheregulationofcellstressresponse AT vadimkumeiko p53familymemberp73intheregulationofcellstressresponse AT alexanderkagansky p53familymemberp73intheregulationofcellstressresponse AT gerrymelino p53familymemberp73intheregulationofcellstressresponse AT carloganini p53familymemberp73intheregulationofcellstressresponse AT nikolaiabarlev p53familymemberp73intheregulationofcellstressresponse |
| _version_ |
1718429429667987456 |