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. 2022 Sep 3;23(17):10104. doi: 10.3390/ijms231710104

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Tumorigenic and pro-metastatic mechanisms of AMPs on gynecological cancers: (1) HBD3 and elafin activate NF-κB pathway [12,95]; (2) Elafin, S100A7 and SLPI induce MEK/ERK pathway [58,68,87,95,96]; (3) SLPI promotes extracellular matrix remodeling and angiogenesis [68,97]; (4) LL-37 and S100A7 induce epithelial-mesenchymal transition (EMT) [58,98]; (5) HE4 controls cell cycle [91]; (6) A vicious circle between macrophages and ovarian cancer cells by interaction between LL-37 and versican V1 [99]. MEK, Mitogen-activated protein kinases; ERK, Extracellular signal-regulated kinases; RAGE, Receptor for advanced glycation end-products; EMT, Epithelial–mesenchymal transition; VDR, vitamin D receptor; TLR, Toll-like receptor; MMP, Matrix metalloproteinases; CYP27B1, Cytochrome P450 family 27 subfamily B member 1.