Unravelling mechanisms of p53-mediated tumour suppression
By K. Bieging, Stephano S. Mello, L. Attardi. Nature Reviews. Cancer, 2014
1,272 citations recorded by the source corpus.
p53 is a crucial tumour suppressor that responds to diverse stress signals by orchestrating specific cellular responses, including transient cell cycle arrest, cellular senescence and apoptosis, which are all processes associated with tumour suppression. However, recent studies have challenged the relative importance of these canonical cellular responses for p53-mediated tumour suppression and have highlighted roles for p53 in modulating other cellular processes, including metabolism, stem cell maintenance, invasion and metastasis, as well as communication within the tumour microenvironment. In this Opinion article, we discuss the roles of classical p53 functions, as well as emerging p53-regulated processes, in tumour suppression.
Subfields: Biotechnology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/fdcb294df7cff9372ca6236a1c69e20b50428ca2
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Citations in the corpus
- Mechanisms of ferroptosis (2016, background): “Moreover, p53 is known to induce the expression of a number of antioxidant genes that would be predicted to suppress ROS accumulation, and therefore counteract ferroptosis [70].”
- The Development of the Concept of Ferroptosis (2018, neutral): “mediated activity of tumor suppression [226,227].”
- The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity. (2017, positive): “…1692–1704, August 15, 2017 ª 2017 The Autho This is an open access article under the CC BY-NC-ND license (http:// arrest and apoptosis under different stress stimuli through transcriptional and transcription-independent mechanisms (Bieging et al., 2014; Green and Kroemer, 2009; Khoo et al., 2014).”
- Oxidative Stress in Cancer (2020, background): “TP53 protects against tumorigenesis primarily by controlling expression of genes involved in cellcycle arrest, senescence, and apoptosis (Bieging et al., 2014).”