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Updated: Sep 26, 2026

Spheroid Assay to Measure TGF-β-induced Invasion
Published on: November 16, 2011
TGF-beta and cancer
1Department of Medicine (Medical Oncology) and Yale Cancer Center, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, CT, USA.
Abstract:
The relationships between transforming growth factor-beta (TGF-beta) and cancer are varied and complex. The paradigm that is emerging from the experimental evidence accumulated over the past decade or so is that TGF-beta can play two different and opposite roles with respect to the process of malignant progression. During early stages of carcinogenesis, TGF-beta acts predominantly as a potent tumor suppressor and may mediate the actions of chemopreventive agents such as retinoids and nonsteroidal anti-estrogens. However, at some point during the development and progression of malignant neoplasms, bioactive TGF-betas make their appearance in the tumor microenvironment and the tumor cells escape from TGF-beta-dependent growth arrest. In many cases, this resistance to TGF-beta is the consequence of loss or mutational inactivation of the genes that encode signaling intermediates. These include the types I and II TGF-beta receptors, as well as receptor-associated and common-mediator Smads. The stage of tumor development or progression at which TGF-beta-resistant clones come to dominate the tumor cell population in different types of neoplasm remains to be defined. The phenotypic switch from TGF-beta-sensitivity to TGF-beta-resistance that occurs during carcinogenesis has several important implications for cancer prevention and treatment.
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