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Effects on mRNA levels of a Numb and Numb-like conditional knockout in skeletal muscle fibers

ABSTRACT: We investigated the gene expression changes resulting from loss of Numb from skeletal muscle fibers using a conditional, inducible knockout of Numb and its close homolog Numb-like (NumbL) bulk RNA-sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE167390 | GEO | 2022/02/16

REPOSITORIES: GEO

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Effects on mRNA levels of a Numb and Numb-like conditional knockout in skeletal muscle fibers

Project description:Effects on mRNA levels of a Numb and Numb-like conditional knockout in skeletal muscle fibers

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Regulation of NUMB alternative splicing by RBM5, RBM6 and RBM10 controls cancer cell proliferation

Project description:RBM5, a regulator of alternative splicing of apoptotic genes, and its close homologues, RBM6 and RBM10, are RNA binding proteins frequently deleted or mutated in lung cancer. We report that RBM5/6 and RBM10 antagonistically regulate the proliferative capacity of cancer cells and display distinct positional effects in alternative splicing regulation. We identify the Notch pathway regulator NUMB as a key target of these factors in the control of cell proliferation. NUMB alternative splicing, which is frequently altered in lung cancer, can regulate colony and xenograft tumor formation and its modulation recapitulates or antagonizes the effects of RBM5, 6 and 10 in cell colony formation. RBM10 mutations identified in lung cancer cells disrupt NUMB splicing regulation to promote cell growth. Our results reveal a key genetic circuit in the control of cancer cell proliferation.

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Project description:Numb is an endocytic adaptor protein that functions in the endocytosis and intracellular trafficking of membrane receptors and adhesion molecules. Numb localization and function have been shown to be regulated by phosphorylation through atypcial protein kinase C at several key sites. Here, we use Liquid Chromatogrpahy, Tandem Mass Spectrometry to identify additional Numb phosphorylation sites not yet characterized.

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Regulation of NUMB alternative splicing by RBM5, RBM6 and RBM10 controls cancer cell proliferation

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numb and numblike deleted by Nkx2.5Cre

Project description:The ventricular wall of the heart is composed of trabeculated and compactlayers, which are separated by yet unknown processes during embryonic development. Notch signaling plays important roles in cardiac development. Mutations in Notch signaling components are related to human congenital heart diseases Two homologues, Numb and Numblike (Numbl), are expressed in mammals, which also act as inhibitors of Notch signaling Here we investigate the role of Notch2 and Numb/Numblike during myocardial trabeculation and compaction. The aim of the experiment is to analyze whether Numb/Numblike are involved in inhibition of Notch activity in the developing heart.

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Loss of NUMB drives aggressive bladder cancer via a RHOA/ROCK/YAP signaling axis.

Project description:We have discovered a previously uncharacterized tumor suppressor function of Numb in the homeostasis of the normal bladder mucosa. Targeted ablation of Numb in the basal layer of the urothelium drives spontaneous bladder tumorigenesis, driving progression from preneoplastic to preinvasive and overtly invasive tumors, and accelerates tumorigenesis in the presence of oncogenic insults. Using 3D-Matrigel organoid cultures to recapitulate bladder tumorigenesis in vitro, we found that Numb deficiency enhances the proliferative and invasive potential of both mouse and human bladder cancer cells. Integrative transcriptomic and functional analyses revealed that downregulation of the canonical Hippo pathway, resulting in enhanced YAP transcriptional activity, underlies the biological aggressiveness of Numb-deficient bladder cancer. These molecular events are dependent on the activation of RhoA/ROCK signaling subsequent to Numb loss. Thus, a dysfunctional Numb–RhoA/ROCK–Hippo/YAP regulatory network is at play in aggressive Numb-deficient bladder cancers, opening avenues for the development of targeted therapies. Furthermore, retrospective cohort studies revealed that a Numb-deficient status correlates with worse overall survival in post-cystectomy muscle-invasive bladder cancer (MIBC) patients and increased risk of progression to MIBC in non-muscle-invasive bladder cancer (NMIBC) patients. The Numb-deficient status was associated with a 27-gene prognostic signature that has the potential to identify high-risk NMIBC patients who are eligible for targeted RhoA/ROCK/YAP therapies.

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