New Insights of TGF-Beta Signaling in Cancer

Dear Colleagues,

Transforming the growth factor (TGF)-β plays a pivotal role in the control of different cellular processes, including proliferation, cell death, differentiation, and migration during both embryonic development and adulthood. Unsurprisingly, the dysregulation of its expression and the altered activation of its intracellular signaling pathways contribute to human diseases, such as tissue fibrosis and cancer. During tumorigenesis, TGF-β may have anticancer activity at early stages, mainly due to its strong antiproliferative effects; however, increasing evidence suggests that the mutational inactivation of the canonical Smad pathway with the concurrent overactivation of non-canonical Smad and non-Smad pathways could contribute to tumor progression at later stages, i.e., by favoring immune suppression, cell invasion, and metastasis. Authors are invited to submit manuscripts that show the possible alterations of these pathways and how they interact with each other in tumor cells. The data may provide useful information on how to better and more selectively target TGF-β signaling for inhibition in various types of human cancer with the goal to improve the prognosis of cancer patients.

In this Special Issue, we aim to shed light on the state-of-the-art and novel data that help to increase our knowledge on the role of TGF-β signaling in the development and progression of human cancer. We welcome experts in the field to contribute research papers and critical reviews on the various facets of TGF-β signaling that either suppress or promote cancer development, as well as on how natural and pharmacological pathway inhibitors for TGF-β signaling, may be exploited as tools in anti-cancer therapies.

Prof. Dr. Hendrik Ungefroren
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• cancer
• TGF-beta
• signaling crosstalk
• smad signaling, non-Smad signaling
• TGF-beta receptors
• TGF-beta signaling inhibitors
• TGF-beta paradox
• epithelial-mesenchymal transition (EMT)
• mesenchymal-epithelial transition (MET)