Transforming growth factor-β enhances matrix metalloproteinase-2 expression and activity through AKT in fibroblasts derived from angiofibromas in patients with tuberous sclerosis complex

Abstract

There is an increase of MMP-2 as a result of TGF-β acting through AKT in TSC tumour cells. This regulation of the TGF-β-AKT-MMP-2 axis is independent of mammalian target of rapamycin (mTOR) signalling. In addition to targeting the mTOR pathway, targeting TGF-β simultaneously could block dysregulated tissue remodelling in TSC tumours.