Abstract：
:Merlin encoded by the Nf2 gene is a bona fide tumor suppressor that has been implicated in regulation of both the Hippo-Yap and Rac1-Pak1 pathways. Using genetically engineered murine liver models, we show that co-deletion of Rac1 with Nf2 blocks tumor initiation but paradoxically exacerbates hepatomegaly induced by Nf2 loss, which can be suppressed either by treatment with pro-oxidants or by co-deletion of Yap. Our results suggest that while Yap acts as the central driver of proliferation during Nf2 tumorigenesis, Rac1 primarily functions as an inflammation switch by inducing reactive oxygen species that, on one hand, induce nuclear factor κB signaling and expression of inflammatory cytokines, and on the other activate p53 checkpoint and senescence programs dampening the cyclin D1-pRb-E2F1 pathway. Interestingly, senescence markers are associated with benign NF2 tumors but not with malignant NF2 mutant mesotheliomas, suggesting that senescence may underlie the benign nature of most NF2 tumors.
journal_name
Dev Celljournal_title
Developmental cellauthors
Shi Y,Bollam SR,White SM,Laughlin SZ,Graham GT,Wadhwa M,Chen H,Nguyen C,Vitte J,Giovannini M,Toretsky J,Yi Cdoi
10.1016/j.devcel.2016.09.027subject
Has Abstractpub_date
2016-11-21 00:00:00pages
452-465issue
4eissn
1534-5807issn
1878-1551pii
S1534-5807(16)30677-3journal_volume
39pub_type
杂志文章abstract：:In this issue of Developmental Cell, Yao et al. (2019) disrupt mitochondrial respiration in limb skeletal progenitors by conditionally deleting Tfam in the mouse embryo. They discover that not only is mitochondrial respiration dispensable for embryonic cartilage development, but also its elimination obviates the need ...
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