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Haploinsufficiency of RREB1 causes a Noonan-like syndrome via epigenetic reprogramming of RAS-MAPK pathway genes.

ABSTRACT: RREB1 is an epigenetic regulator of the RAS-MAPK pathway genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE146902 | GEO | 2020/03/13

REPOSITORIES: GEO

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Haploinsufficiency of RREB1 causes a Noonan-like syndrome via epigenetic reprogramming of RAS-MAPK pathway genes.

Project description:Haploinsufficiency of RREB1 causes a Noonan-like syndrome via epigenetic reprogramming of RAS-MAPK pathway genes.

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Haploinsufficiency of RREB1 causes a Noonan-like RASopathy via epigentic regulation of RAS-MAPK pathway genes.

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Haploinsufficiency of RREB1 causes a Noonan-like RASopathy via epigenetic reprogramming of RAS-MAPK pathway genes.

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Haploinsufficiency of RREB1 causes a Noonan-like RASopathy via epigentic regulation of RAS-MAPK pathway genes.

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Effect of RREB1 knockdown using siRNA in A673 Ewing sarcoma cells (RNA-seq)

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RNA-sequencing of Rreb1+/+ and Rreb1-/- embryonic day 7.5 mouse embryos

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Hyperactive RAS/MAPK introduces cancer-specific mitotic vulnerabilities

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TGF-β and RREB1 coordinate EMT programs in development and cancer

Project description:Epithelial-to-mesenchymal transitions (EMT) play prominent roles during development, regeneration and tumor progression. EMTs are triggered by TGF-β, RAS and other signals that cooperatively induce the expression of master EMT transcription factors such as SNAIL. Here, we elucidate how the TGF-β and RAS pathways jointly trigger EMTs and tie them to broader developmental programs. We identify RAS response element binding protein 1 (RREB1) as a critical partner of TGF-β-activated SMAD transcription factors in driving SNAIL expression in pancreatic pre-malignant epithelial cells, lung adenocarcinoma cells, and embryonic stem cells. Moreover, SMADs and RREB1 also drive EMT-associated fibrogenic programs in epithelial cells and mesendoderm differentiation in pluripotent embryonic cells. These findings illuminate the orchestration of EMT associated programs in gastrulation, fibrosis, and cancer.

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Loss of primary cilia drives switching from Hedgehog to Ras/MAPK pathway

Project description:Basal cell carcinomas (BCCs) rely on Hedgehog (HH) pathway growth signal amplification by the microtubule-based organelle, the primary cilium. Despite naïve tumors responsiveness to Smoothened inhibitors (Smoi), resistance in advanced tumors remains frequent. While the resistant BCCs usually maintain HH pathway activation, squamous cell carcinomas with Ras/MAPK pathway activation also arise, with the molecular basis of tumor type and pathway selection still obscure. Here we identify the primary cilium as a critical determinant controlling tumor pathway switching. Strikingly, Smoi-resistant BCCs possess an increased mutational load in ciliome genes, resulting in reduced primary cilia and HH pathway activation compared to naive or Gorlin patient BCCs. Gene set enrichment analysis of resistant BCCs with a low HH pathway signature reveals increased Ras/MAPK pathway activation. Tissue analysis confirms an inverse relationship between primary cilia presence and Ras/MAPK activation, and primary cilia removal in BCCs potentiates Ras/MAPK pathway activation. Moreover, activating Ras in HH-responsive cell lines confers resistance to both canonical (vismodegib) and non-canonical (aPKC and MRTF inhibitors) HH pathway inhibitors, while conferring sensitivity to MAPK inhibitors. Our results provide new insights into BCC treatment and identify the primary cilium as an important lineage gatekeeper, preventing HH to Ras/MAPK pathway switching.

2018-10-10 | GSE120954 | GEO

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