Unremitting Cell Proliferation in the Secretory Phase of Eutopic Endometriosis: Involvement of pAkt and pGSK3β
Endometriosis eutopic endometrium showed increased Ki67 and SCF, with pAkt and pGSK3β remaining overexpressed in the secretory phase compared to controls.
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This study analyzed eutopic endometrium from 35 women with endometriosis and 25 fertile controls with normal cycles, using in situ expression measurements across menstrual phases for SCF/c-kit, Ki67, Akt/GSK3β, and their phosphorylated forms. Ki67 and SCF expression were higher in endometriosis than controls and were greater in the secretory phase rather than the proliferative phase, while c-kit expression was also higher overall but did not differ by phase. In contrast, total Akt and GSK3β levels were identical across all samples, but phosphorylated Akt and phosphorylated GSK3β remained overexpressed in the secretory phase in endometriosis compared with control tissue. The authors’ main limitation is that this is an expression-based, in situ analysis without functional experiments to prove causality. This paper is centrally about endometriosis — it investigates how c-kit/SCF and pAkt/pGSK3β signaling relate to unremitting cell proliferation in the secretory phase of eutopic endometriosis.
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- Human Endometriosis Tissue Microarray Reveals Site-specific Expression of Estrogen Receptors, Progesterone Receptor, and Ki67 2018
- The Wnt/β-catenin signaling in endometriosis, the expression of total and active forms of β-catenin, total and inactive forms of glycogen synthase kinase-3β, WNT7a and DICKKOPF-1 2017
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