PDGFRβ signaling cooperates with β-catenin to modulate c-Abl and biologic behavior of desmoid-type fibromatosis [RNA-seq I]

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UID: 11214

Author(s): Hu, Jia*, Crago, Aimee M.* * MSK affiliated

Description: Summary from GEO:

"The mechanisms underlying oncogenesis in desmoid-type fibromatosis are poorly understood. This project sought to understand how β-catenin may function to promote desmoid formation and how external signaling by PDGFRβ modulates this activity. To examine this question, RNA-seq was performed on CTNNB1 knock-downs. Gene set enrichment analysis suggested that the oncogene controlled HIF1 and angiogenesis pathways; expression of related genes accurately differentiated desmoids analyzed by U133A array from normal mesenchymal tissues. We identified c-ABL as a direct transcriptional target of β-catenin that promoted HIF1α expression in desmoid cells. We also noted that c-ABL activity was enhanced by PDGFRβ. PDGFRβ enhanced desmoid cell proliferation and c-ABL was necessary for desmoid proliferation. To identify potential markers of PDGFRβ/c-ABL activity in vivo, we assessed RNA-seq of desmoid cells treated with PDGF-BB. ERG1 transcription was highly upregulate and IHC of ERG1 was subsequently used to assess outcomes in desmoid patients with biopsies available for testing."

Overall design from GEO:

"1. Primary desmoid cell line DES9525 were treated with shRNA directed against CTNNB1, selected with antibiotic and RNA-seq analyzed on both CTNNB1 knock-downs and scramble controls
2. Primary desmoid cell line DES9525 was treated with PDGF-BB (20ng/ml) for 24 hours and RNA-seq performed on both treated and untreated cells"

Subject of Study

Subject(s)

OncoTree Cancer Type(s)

Desmoid/Aggressive Fibromatosis

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