DC CFAR microgrant awardee, Robert Furler, PhD, along with his colleagues, has published an article in Cancers entitled, "TGF-beta Sustains Tumor Progression through Biochemical and Mechanical Signal Transduction".
This article discusses the results from a study looking at transforming growth factor β (TGF-β) signaling and its role in promoting tumor growth. TGF-β) signaling can dampen immune responses during cancer progression through biochemical and mechanical signal transduction pathways. Because TGF-β receptors (TGF-βR's) are found on several cell types, tumor-derived TGF-β can create a pro-tumorigenic microenvironment by influencing the activity of surrounding leukocytes, endothelial cells, and fibroblasts. The researchers reviewed the role ofTGF-β activated kinase 1 (TAK1) activation at the intersection of proinflammatory signaling by immune receptors and anti-inflammatory signaling by TGF-β receptors. Additionally, they examined the role of TGF-β in the mechanobiology of cancer. They concluded that understanding how TGF-β dampens proinflammatory responses and induces pro-survival mechanical signals throughout cancer development is critical for designing therapeutics that inhibit tumor progression while bolstering the immune response.
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