EGF hijacks miR-198/FSTL1 wound-healing switch and steers a two-pronged pathway toward metastasis

Published date : 21 Aug 2017

Epithelial carcinomas are well known to activate a prolonged wound-healing program that promotes malignant transformation. Wound closure requires the activation of keratinocyte migration via a dual-state molecular switch. This switch involves production of either the anti-migratory microRNA miR-198 or the pro-migratory follistatin-like 1 (FSTL1) protein from a single transcript; miR-198 expression in healthy skin is down-regulated in favor of FSTL1 upon wounding, which enhances keratinocyte migration and promotes re-epithelialization.

Journal Paper
The Journal of Experimental Medicine, 2017,doi: 10.1084/jem.20170354
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