Journal
SEMINARS IN CANCER BIOLOGY
Volume 63, Issue -, Pages 36-43Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2019.05.010
Keywords
Cell competition; Cell fitness; Metabolism; Apoptosis; Growth regulation; P53; Myc; Hippo; NF-kappa B; Stat
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Funding
- NHLI foundation PhD studentship
- EMBO long-term fellowship
- Marie Curie international fellowship
- British Heart Foundation PhD studentship
- MRC [MR/N009371/1]
- BHF centre for research excellence
- BBSRC [BB/S008284/1] Funding Source: UKRI
- MRC [MR/P018467/1] Funding Source: UKRI
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The maintenance of tissue homeostasis and health relies on the efficient removal of damaged or otherwise suboptimal cells. One way this is achieved is through cell competition, a fitness quality control mechanism that eliminates cells that are less fit than their neighbours. Through this process, cell competition has been shown to play diverse roles in development and in the adult, including in homeostasis and tumour suppression. However, over the last few years it has also become apparent that certain oncogenic mutations can provide cells with a competitive advantage that promotes their expansion via the elimination of surrounding wild-type cells. Thus, understanding how this process is initiated and regulated will provide important insights with relevance to a number of different research areas. A key question in cell competition is what determines the competitive fitness of a cell. Here, we will review what is known about this question by focussing on two non-mutually exclusive possibilities; first, that the activity of a subset of transcription factors determines competitive fitness, and second, that the outcome of cell competition is determined by the relative cellular metabolic status.
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