Sundaram Gopinath M, Sampath Prabha
Institute of Medical Biology, Agency for Science Technology & Research (ASTAR), Singapore 138648.
Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Mol Cell Oncol. 2018 Sep 20;5(6):e1432255. doi: 10.1080/23723556.2018.1432255. eCollection 2018.
Wound healing is a dynamic event where barrier disruption is transient and miR-198/FSTL1 molecular switch orchestrate wound re-epithelialization. However, epithelial carcinomas maintain a prolonged wound-healing phase to promote malignant transformation. Delineating the molecular mechanism we demonstrate, how epidermal growth factor (EGF) hijacks the wound-healing switch to promote metastasis of carcinoma.
伤口愈合是一个动态过程,在此过程中屏障破坏是短暂的,且miR-198/FSTL1分子开关协调伤口的重新上皮化。然而,上皮癌维持一个延长的伤口愈合阶段以促进恶性转化。我们阐述了分子机制,即表皮生长因子(EGF)如何劫持伤口愈合开关来促进癌转移。