Journal
FRONTIERS IN MOLECULAR BIOSCIENCES
Volume 9, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fmolb.2022.991612
Keywords
transforming growth factor-b (TGFb); Smad; receptor trafficking; epithelial-mesenchymal transition (EMT); autophagy; protein 62; sequestosome 1 (p62; SQSTM1)
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This article reviews the TGF beta signaling pathways, the biological effects of TGF beta in tumorigenesis, and how protein quality control pathways contribute to the tumor-promoting outcomes of TGF beta signaling.
Transforming growth factor-beta (TGF beta) is a ubiquitous cytokine essential for embryonic development and postnatal tissue homeostasis. TGF beta signalling regulates several biological processes including cell growth, proliferation, apoptosis, immune function, and tissue repair following injury. Aberrant TGF beta signalling has been implicated in tumour progression and metastasis. Tumour cells, in conjunction with their microenvironment, may augment tumourigenesis using TGF beta to induce epithelial-mesenchymal transition, angiogenesis, lymphangiogenesis, immune suppression, and autophagy. Therapies that target TGF beta synthesis, TGF beta-TGF beta receptor complexes or TGF beta receptor kinase activity have proven successful in tissue culture and in animal models, yet, due to limited understanding of TGF beta biology, the outcomes of clinical trials are poor. Here, we review TGF beta signalling pathways, the biology of TGF beta during tumourigenesis, and how protein quality control pathways contribute to the tumour-promoting outcomes of TGF beta signalling.
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