Transforming growth factor-β (TGF-β) plays a dual role in cancer development and progression. On one hand, TGF-β can suppress tumorigenesis by inhibiting cell cycle progression and inducing apoptosis. On the other hand, it can modulate cancer-related processes such as cell invasion, distant metastasis, and microenvironment modification, which may be exploited by cancer cells for their advantage. The correlation between TGF-β expression and cancer prognosis has been extensively investigated, with high TGF-β levels often associated with poor outcomes. However, the relationship is not always straightforward, and the mechanisms underlying these effects are complex. TGF-β can inhibit cell cycle progression through the induction of p15INK4b, p21Cip1, p16INK4a, and p19ARF, and by suppressing c-MYC and ID proteins. It can also induce apoptosis through pathways involving DAXX, DAP-kinase, and ARTS. In malignant cells, TGF-β can be used to promote angiogenesis, immune system suppression, and epithelial-to-mesenchymal transition (EMT), enhancing tumor progression. The disruption of the canonical TGF-β/Smad signaling pathway can lead to tumor formation, and mutations in TGF-β receptors can further enhance tumor growth. TGF-β inhibitors are being explored as potential therapeutic targets, with early clinical trials showing promising efficacy and safety. However, the optimal timing and combination of TGF-β blockade with other therapies remain areas of ongoing research.Transforming growth factor-β (TGF-β) plays a dual role in cancer development and progression. On one hand, TGF-β can suppress tumorigenesis by inhibiting cell cycle progression and inducing apoptosis. On the other hand, it can modulate cancer-related processes such as cell invasion, distant metastasis, and microenvironment modification, which may be exploited by cancer cells for their advantage. The correlation between TGF-β expression and cancer prognosis has been extensively investigated, with high TGF-β levels often associated with poor outcomes. However, the relationship is not always straightforward, and the mechanisms underlying these effects are complex. TGF-β can inhibit cell cycle progression through the induction of p15INK4b, p21Cip1, p16INK4a, and p19ARF, and by suppressing c-MYC and ID proteins. It can also induce apoptosis through pathways involving DAXX, DAP-kinase, and ARTS. In malignant cells, TGF-β can be used to promote angiogenesis, immune system suppression, and epithelial-to-mesenchymal transition (EMT), enhancing tumor progression. The disruption of the canonical TGF-β/Smad signaling pathway can lead to tumor formation, and mutations in TGF-β receptors can further enhance tumor growth. TGF-β inhibitors are being explored as potential therapeutic targets, with early clinical trials showing promising efficacy and safety. However, the optimal timing and combination of TGF-β blockade with other therapies remain areas of ongoing research.