RT Journal Article
T1 Oncogenic pathways activated by pro-inflammatory cytokines promote mutant p53 stability: clue for novel anticancer therapies
A1 D'Orazi, Gabriella
A1 Cordani, Marco
A1 Cirone, Mara
AB Inflammation and cancerogenesis are strongly interconnected processes, not only because inflammation promotes DNA instability, but also because both processes are driven by pathways such as NF-kB, STAT3, mTOR and MAPKs. Interestingly, these pathways regulate the release of pro-inflammatory cytokines such as IL-6, TNF-α and IL-1β that in turn control their activation and play a crucial role in shaping immune response. The transcription factor p53 is the major tumor suppressor that is often mutated in cancer, contributing to tumor progression. In this overview, we highlight how the interplay between pro-inflammatory cytokines and pro-inflammatory/pro-oncogenic pathways, regulating and being regulated by UPR signaling and autophagy, affects the stability of mutp53 that in turn is able to control autophagy, UPR signaling, cytokine release and the activation of the same oncogenic pathways to preserve its own stability and promote tumorigenesis. Interrupting these positive feedback loops may represent a promising strategy in anticancer therapy, particularly against cancers carrying mutp53.
PB Springer Nature
SN 1420-9071
YR 2020
FD 2020
LK https://hdl.handle.net/20.500.14352/97795
UL https://hdl.handle.net/20.500.14352/97795
LA eng
NO D’Orazi, G., Cordani, M. & Cirone, M. Oncogenic pathways activated by pro-inflammatory cytokines promote mutant p53 stability: clue for novel anticancer therapies. Cell. Mol. Life Sci. 78, 1853–1860 (2021). https://doi.org/10.1007/s00018-020-03677-7
NO Italian Association for Cancer Research
NO Pasteur Institute (Italy)
DS Docta Complutense
RD 10 abr 2025