Abstract
As extracellular matrix receptors that mediate both ‘inside-out’ and ‘outside-in’ signaling, integrins on tumor cells control reciprocal interactions with the tumor microenvironment (TME) that drive tumor growth and progression. However, therapeutic strategies to target integrins are hindered by incomplete understanding of their complex roles in TME modulation. Mice with constitutive Itga3 deletion in epidermis show greatly reduced skin tumors in the 2-step chemical tumorigenesis model, indicating a pro-tumorigenic role for integrin α3β1.
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