Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA121917 | ENA |
REPOSITORIES: ENA
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Project description:Meningiomas are the most common primary brain tumors, where complete surgical resection is often challenging giving rise to recurrence. Mutations of the E3 ubiquitin ligase TRAF7 are found in one-fourth of meningioma patients and typically co-occur with mutations in either KLF4, AKT1, or PI3KCA. By creating an in vitro meningioma model derived from primary meningeal cells, we elucidated the cooperative interactions that conspire meningioma development. A multi-omics framework on meningeal cells revealed TRAF7-mediated rewiring of the proteome with the majority of protein expression being post‐transcriptionally‐regulated. Integrating TRAF7-driven ubiquitinome and proteome alterations and TRAF7 interactome highlight the role of TRAF7 in posttranslational regulation of the cytoskeleton organization. TRAF7 controls actin dynamics by acting as a proteostatic regulator of the RAS-related small GTPases. TRAF7 loss-of-function diminishes ubiquitination of RAS and CDC42, leading to the activation of the PAK and MAPK signaling pathways. Up-regulation of CDC42 signaling promotes anchorage-independent growth of meningeal cells. On the other hand, the RAS/MAPK pathway triggers the tumor suppressive activity of KLF4 that inhibits meningeal cell growth due to the activation of the Semaphorin pathway. Simultaneous loss of KLF4 and TRAF7 function enhances tumorigenic transformation of meningeal cells, functionally confirming their roles in meningioma development.
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Project description:Meningiomas are the most common primary brain tumors, where complete surgical resection is often challenging giving rise to recurrence. Mutations of the E3 ubiquitin ligase TRAF7 are found in one-fourth of meningioma patients and typically co-occur with mutations in either KLF4, AKT1, or PI3KCA. By creating an in vitro meningioma model derived from primary meningeal cells, we elucidated the cooperative interactions that conspire meningioma development. A multi-omics framework on meningeal cells revealed TRAF7-mediated rewiring of the proteome with the majority of protein expression being post‐transcriptionally‐regulated. Integrating TRAF7-driven ubiquitinome and proteome alterations and TRAF7 interactome highlight the role of TRAF7 in posttranslational regulation of the cytoskeleton organization. TRAF7 controls actin dynamics by acting as a proteostatic regulator of the RAS-related small GTPases. TRAF7 loss-of-function diminishes ubiquitination of RAS and CDC42, leading to the activation of the PAK and MAPK signaling pathways. Up-regulation of CDC42 signaling promotes anchorage-independent growth of meningeal cells. On the other hand, the RAS/MAPK pathway triggers the tumor suppressive activity of KLF4 that inhibits meningeal cell growth due to the activation of the Semaphorin pathway. Simultaneous loss of KLF4 and TRAF7 function enhances tumorigenic transformation of meningeal cells, functionally confirming their roles in meningioma development.
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Project description:Meningiomas are common brain tumours arising from meningeal tissue. Despite the majority of them displaying benign features, they can cause mild to severe morbidity. The current main therapeutic approach is complete tumour resection commonly with adjunct radiation therapy. However, tumour location can hamper complete resection and chemotherapies are ineffective. In this study we aim to elucidate dysregulated pathways in meningioma pathogenesis and identify novel molecular targets by deciphering the proteome and phosphoproteome of different grades of meningiomas. Tumour lysates were collected from grade I, II and III frozenmeningioma specimens and three normal healthy human meninges.
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Project description:Meningiomas are common brain tumours arising from meningeal tissue. Despite the majority of them displaying benign features, they can cause mild to severe morbidity. The current main therapeutic approach is complete tumour resection commonly with adjunct radiation therapy. However, tumour location can hamper complete resection and chemotherapies are ineffective. In this study we aim to elucidate dysregulated pathways in meningioma pathogenesis and identify novel molecular targets by deciphering the proteome and phosphoproteome of different grades of meningiomas. Tumour lysates were collected from grade I, II and III frozemeningioma specimens and three normal healthy human meninges.
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