ArticleEMBO molecular medicine2010
p21 loss blocks senescence following Apc loss and provokes tumourigenesis in the renal but not the intestinal epithelium.
Article in EMBO molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
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- TGFβ inhibition restores a regenerative response in acute liver injury by suppressing paracrine senescence.Science translational medicine · 2018Article
- Mbd2 enables tumourigenesis within the intestine while preventing tumour-promoting inflammation.The Journal of pathology · 2018Article
- TGFβ pathway limits dedifferentiation following WNT and MAPK pathway activation to suppress intestinal tumourigenesis.Cell death and differentiation · 2017Article
- Cellular senescence in renal ageing and disease.Nature reviews. Nephrology · 2017Review
- Distinct Transcriptional Changes and Epithelial-Stromal Interactions Are Altered in Early-Stage Colon Cancer Development.Molecular cancer research : MCR · 2016Article
- The role of HIF1α in renal cell carcinoma tumorigenesis.Journal of molecular medicine (Berlin, Germany) · 2014Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Senescence has been implicated as an important mechanism of tumour suppression in a number of human malignancies, including colorectal cancer (CRC). However, we still have a relatively poor understanding of how the underlying mutations that occur in cancer cause senescence and its relevance in vivo. The Apc gene is mutated in approximately 80% of CRC as the initiating event, but rarely elsewhere. In this study we have examined the capacity of Apc loss to induce senescence in the intestinal epithelium compared to the renal epithelium. Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. Within the intestinal epithelium, loss of Apc did not induce senescence. Moreover, combined Apc and p21 or Ink4A loss had no impact upon tumourigenesis. Taken together, these results show that Apc loss in vivo invokes a senescence program in a context-dependent fashion, and implies senescence may play a key barrier to tumourigenesis in the kidney. However, in CRC, escape from senescence is likely to only be a barrier in cancers initiated by other mutations.
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