Epgn, also known as epithelial mitogen, is an epidermal growth factor receptor (EGFR) ligand. As an EGFR ligand, it is involved in the EGFR signaling pathway, which regulates many crucial cellular programs such as cell proliferation, differentiation, and survival [1,2]. It has been shown to have significant biological importance in processes related to cell growth regulation and tissue homeostasis.

Epgn was first identified in granulosa cells as rapidly induced by LH/hCG and was demonstrated to initiate cumulus expansion, similar to other EGF-receptor ligands [6]. In a contact dermatitis model, curcumin was found to inhibit the upregulation of Epgn by 2,4,6-trinitrochlorobenzene, which was associated with attenuation of skin swelling, suggesting Epgn's role in the cell proliferation and swelling processes in this context [4]. In a mucosal damage model in larval zebrafish, transcriptional profiling identified significant upregulation of Epgn upon mucosal damage, and treatment with recombinant human Epgn suppressed epithelial cell extrusion, leading to reduced fungal invasion and enhanced survival [5]. In lung cancer, the interaction between epithelial mitogen (EPGN)-EGFR was supported through spatial distribution analysis, revealing the significant proximity between EPGN+ mesothelial cells and EGFR+ epithelial cells, highlighting its role in pleural metastasis [3].

In conclusion, Epgn plays essential roles in multiple biological processes including ovarian function, skin inflammation response, mucosal defense, and cancer metastasis through its interaction with the EGFR pathway. Studies related to Epgn in these areas, especially those using in-vivo models, contribute to understanding the molecular mechanisms underlying these biological processes and diseases, potentially providing new therapeutic targets.

References:

1. Freed, Daniel M, Bessman, Nicholas J, Kiyatkin, Anatoly, Lidke, Diane S, Lemmon, Mark A. 2017. EGFR Ligands Differentially Stabilize Receptor Dimers to Specify Signaling Kinetics. In Cell, 171, 683-695.e18. doi:10.1016/j.cell.2017.09.017. https://pubmed.ncbi.nlm.nih.gov/28988771/

2. Singh, Bhuminder, Carpenter, Graham, Coffey, Robert J. 2016. EGF receptor ligands: recent advances. In F1000Research, 5, . doi:10.12688/f1000research.9025.1. https://pubmed.ncbi.nlm.nih.gov/27635238/

3. Li, Pei-Heng, Zhang, Xin, Yan, Huayun, Li, Zhi-Hui, Shu, Yang. 2024. Contribution of crosstalk of mesothelial and tumoral epithelial cells in pleural metastasis of lung cancer. In Translational lung cancer research, 13, 965-985. doi:10.21037/tlcr-24-118. https://pubmed.ncbi.nlm.nih.gov/38854934/

4. Sakai, Hiroyasu, Sato, Ken, Sato, Fumiaki, Narita, Minoru, Chiba, Yoshihiko. 2017. Curcumin inhibits epigen and amphiregulin upregulated by 2,4,6-trinitrochlorobenzene associated with attenuation of skin swelling. In Inflammation research : official journal of the European Histamine Research Society ... [et al.], 66, 663-678. doi:10.1007/s00011-017-1048-0. https://pubmed.ncbi.nlm.nih.gov/28405735/

5. Wurster, Sebastian, Ruiz, Oscar E, Samms, Krystin M, Kontoyiannis, Dimitrios P, Eisenhoffer, George T. . EGF-mediated suppression of cell extrusion during mucosal damage attenuates opportunistic fungal invasion. In Cell reports, 34, 108896. doi:10.1016/j.celrep.2021.108896. https://pubmed.ncbi.nlm.nih.gov/33761358/

6. Carletti, Martha Z, Christenson, Lane K. 2009. Rapid effects of LH on gene expression in the mural granulosa cells of mouse periovulatory follicles. In Reproduction (Cambridge, England), 137, 843-55. doi:10.1530/REP-08-0457. https://pubmed.ncbi.nlm.nih.gov/19225042/