This review elaborates on the dualistic roles of Transforming Growth Factor-β (TGF-β) in cancer, illustrating its transition from a tumor suppressor in early cancer stages to a promoter of tumor progression in advanced stages. Initially, TGF-β inhibits tumor growth by suppressing cellular proliferation and inducing apoptosis. However, as tumors evolve, they often develop resistance to TGF-β’s suppressive effects, at which point TGF-β promotes tumor progression by enhancing invasion, metastasis, and angiogenesis. This shift is due to changes in the tumor microenvironment and the cellular context, which alter TGF-β signaling pathways.
The understanding of TGF-β's shifting roles in cancer provides valuable insights for Novastem’s stem cell therapies. Similar to how TGF-β can switch from a suppressive to a promoting factor in cancer, stem cell therapies might be optimized by modulating TGF-β signaling to support tissue regeneration in early stages while avoiding potential pro-tumorigenic effects in later stages or in different contexts.
Early Suppression, Late Promotion: TGF-β functions as a tumor suppressor in early-stage cancers but promotes metastasis and angiogenesis in advanced cancers.
Therapeutic Targeting: Strategies to inhibit TGF-β’s pro-tumorigenic effects include ligand traps, receptor kinase inhibitors, and antisense oligonucleotides, each with distinct mechanisms and implications for therapy.
TGF-β and Stem Cells: Insights into TGF-β signaling can guide the development of stem cell therapies, potentially using TGF-β modulators to enhance the regenerative properties or to inhibit undesirable pathways.
This review elaborates on the dualistic roles of Transforming Growth Factor-β (TGF-β) in cancer, illustrating its transition from a tumor suppressor in early cancer stages to a promoter of tumor progression in advanced stages. Initially, TGF-β inhibits tumor growth by suppressing cellular proliferation and inducing apoptosis. However, as tumors evolve, they often develop resistance to TGF-β’s suppressive effects, at which point TGF-β promotes tumor progression by enhancing invasion, metastasis, and angiogenesis. This shift is due to changes in the tumor microenvironment and the cellular context, which alter TGF-β signaling pathways.
The understanding of TGF-β's shifting roles in cancer provides valuable insights for Novastem’s stem cell therapies. Similar to how TGF-β can switch from a suppressive to a promoting factor in cancer, stem cell therapies might be optimized by modulating TGF-β signaling to support tissue regeneration in early stages while avoiding potential pro-tumorigenic effects in later stages or in different contexts.
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