Corrigendum to “Corticosteroids stimulate selectively transforming growth factor (TGF)-β receptor type III expression in transdifferentiating hepatic stellate cells”[J Hepatol 40 (2004) 69–76]

Wickert, Lucia; Abiaka, M.; Bolkenius, Ursula; Gressner, A. M.

doi:10.1016/j.jhep.2003.09.030

Cited by 1 publication

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“…At the transcriptional level, TβRIII expression is negatively regulated by TGF-β1 through inhibition of the proximal promoter in multiple cell types, including breast, ovarian, and small cell lung cancer cell lines, as well as by bone morphogenetic protein-2 (BMP-2) in osteoblast cell lines [20, 28-29]. Expression of TβRIII mRNA has also been reported to decrease with transdifferentiation of hepatic stellate cells (HSC) to myofibroblasts [30] and during induction of EMT in a pancreatic model [16]. In contrast corticosteroids, specifically dexamethasone, aldosterone, and hydrocortisone, transcriptionally up-regulate TβRIII mRNA expression in hepatic stellate cells (HSCs), myofibroblasts, and osteoblasts while both MyoD and retinoic acid increase TβRIII expression in mouse myoblast cells [28-31].…”

Section: Regulation Structure and Function Of The Type III Tgf-β Rementioning

confidence: 99%

Roles for the type III TGF-β receptor in human cancer

Gatza

Blobe

2010

Cellular Signalling

160

176

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Transforming growth factor β (TGF-β) superfamily ligands have important roles in regulating cellular homeostasis, embryonic development, differentiation, proliferation, immune surveillance, angiogenesis, motility, and apoptosis in a cell type and context specific manner. TGF-β superfamily signaling pathways also have diverse roles in human cancer, functioning to either suppress or promote cancer progression. The TGF-β superfamily co-receptor, the type III TGF-β receptor (TβRIII, also known as betaglycan) mediates TGF-β superfamily ligand dependent as well as ligand independent signaling to both Smad and non-Smad signaling pathways. Loss of TβRIII expression during cancer progression and direct effects of TβRIII on regulating cell migration, invasion, proliferation, and angiogenesis support a role for TβRIII as a suppressor of cancer progression and/or as a metastasis suppressor. Defining the physiological function and mechanism of TβRIII action and alterations in TβRIII function during cancer progression should enable more effective targeting of TβRIII and TβRIII mediated functions for the diagnosis and treatment of human cancer.

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