The TGF-β Family in Glioblastoma

The TGF-β Family in Glioblastoma

15 January 2024 | Irene Golán-Cancela and Laia Caja
The TGF-β family plays a critical role in glioblastoma (GBM) biology, with TGF-β promoting tumorigenesis and BMPs suppressing it by inducing tumor cell differentiation. GBM is the most common malignant brain tumor in adults, with a median survival of 15 months despite current treatments. TGF-β signaling is involved in GBM progression, including cancer stem cell (CSC) maintenance, tumor microenvironment (TME) regulation, and immune evasion. TGF-β induces EMT, promotes tumor cell invasion, and suppresses immune responses, while BMPs promote differentiation and inhibit tumor growth. TGF-β signaling is modulated by various factors, including deubiquitinating enzymes and miRNAs, and its dysregulation contributes to GBM progression. BMPs also play a role in GBM by promoting differentiation and suppressing tumor growth. Therapeutic strategies targeting TGF-β and BMP signaling are being explored, including monoclonal antibodies, small-molecule inhibitors, and gene therapy approaches. Despite these efforts, GBM remains challenging to treat due to the blood-brain barrier and the complex tumor microenvironment. Current research focuses on improving drug delivery, targeting TGF-β signaling, and combining therapies to enhance treatment outcomes in GBM patients.The TGF-β family plays a critical role in glioblastoma (GBM) biology, with TGF-β promoting tumorigenesis and BMPs suppressing it by inducing tumor cell differentiation. GBM is the most common malignant brain tumor in adults, with a median survival of 15 months despite current treatments. TGF-β signaling is involved in GBM progression, including cancer stem cell (CSC) maintenance, tumor microenvironment (TME) regulation, and immune evasion. TGF-β induces EMT, promotes tumor cell invasion, and suppresses immune responses, while BMPs promote differentiation and inhibit tumor growth. TGF-β signaling is modulated by various factors, including deubiquitinating enzymes and miRNAs, and its dysregulation contributes to GBM progression. BMPs also play a role in GBM by promoting differentiation and suppressing tumor growth. Therapeutic strategies targeting TGF-β and BMP signaling are being explored, including monoclonal antibodies, small-molecule inhibitors, and gene therapy approaches. Despite these efforts, GBM remains challenging to treat due to the blood-brain barrier and the complex tumor microenvironment. Current research focuses on improving drug delivery, targeting TGF-β signaling, and combining therapies to enhance treatment outcomes in GBM patients.
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