AI Article Synopsis
- Cellular senescence can stop tumors by putting cells into a permanent growth halt but can also help tumors grow by changing the surrounding environment.
- In adamantinomatous craniopharyngioma (ACP), senescent cells with a specific mutation produce signals (SASP) that may help initiate and support tumor growth.
- Research suggests that this process of paracrine signaling from senescent cells could be important in the development of many types of tumors, not just ACP.
Article Abstract
Cellular senescence is a process that can prevent tumour development in a cell autonomous manner by imposing a stable cell cycle arrest after oncogene activation. Paradoxically, senescence can also promote tumour growth cell non-autonomously by creating a permissive tumour microenvironment that fuels tumour initiation, progression to malignancy and metastasis. In a pituitary tumour known as adamantinomatous craniopharyngioma (ACP), cells that carry oncogenic β-catenin mutations and overactivate the WNT signalling pathway form cell clusters that become senescent and activate a senescence-associated secretory phenotype (SASP). Research in mouse models of ACP has provided insights into the function of the senescent cell clusters and revealed a critical role for SASP-mediated activities in paracrine tumour initiation. In this review, we first discuss this research on ACP and subsequently explore the theme of paracrine tumourigenesis in other tumour models available in the literature. Evidence is accumulating supporting the notion that paracrine signalling brought about by senescent cells may underlie tumourigenesis across different tumours and cancer models.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8195904 | PMC |
| http://dx.doi.org/10.1007/s00018-021-03798-7 | DOI Listing |
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