However, patient survival data from REMBRANDT database reveals a highly significant link between THBS1 overexpression and poor survival rates ( Figure 6b ). 32 We speculate that THBS1 acts as an oncogene via activation of latent TGF- β in the extracellular environment. 40 Downregulation of pro-angiogenic Notch ligand, JAG1, enables NOTCH1 receptor to act as a tumor suppressor via its sequestration of CTNNB1, hence avoiding conflict with its potential angiogenic contribution via JAG1 activation.
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MicroRNA-10b pleiotropically regulates invasion, angiogenicity and apoptosis of tumor cells resembling mesenchymal subtype of glioblastoma multiforme.
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