Augmented cell survival in eutopic endometrium from women with endometriosis: Expression of c-myc, TGF-beta1 and bax genes

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AI-generated summary by claude@2026-06, 2026-06-07

Eutopic endometrium from women with endometriosis showed increased cell proliferation and reduced apoptosis, with altered expression of c-myc, TGF-beta1, and bax genes, suggesting enhanced cell survival.

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AI-generated deep summary by claude@2026-06, 2026-06-07

This study evaluated how proliferation and apoptosis are balanced across the menstrual cycle in eutopic endometrium from 30 women with endometriosis versus 34 fertile control women, measuring TUNEL-based apoptosis, Ki67 proliferation, and mRNA/protein expression of bax, c-myc, and TGF-beta1 using endometrial explants and RT-PCR/IHC. Proliferation in glands decreased from proliferative to late secretory phases in both groups, but endometriosis-associated endometrium showed higher Ki67 positivity in both glands and stroma during the proliferative phase, alongside higher c-myc mRNA (65% increase). TGF-beta1 mRNA and protein increased during mid-secretory phase in normal endometrium, an effect not seen in endometriosis, and apoptosis-related epithelial/stromal increases in late secretory phase occurred in controls but not in endometriosis; correspondingly, bax mRNA was reduced (63%) in endometriosis, while early secretory phase showed increased apoptotic stromal cells with higher bax mRNA. The paper does not state a specific limitation in the excerpted text beyond describing cycle staging and assay semi-quantification, which may affect generalizability. This paper is centrally about endometriosis — it links altered c-myc, TGF-beta1, and bax expression to reduced apoptosis and augmented survival in eutopic endometrium from women with endometriosis.

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Abstract

BACKGROUND: Endometriosis is a common gynaecological disorder characterized by the presence of endometrial tissue outside of the uterus. The fragments in normal menstruation are composed of necrotic and living cells, which do not survive in ectopic locations because of programmed cell death. The aim of this study was to evaluate if the balance between cell proliferation and apoptosis is changed in eutopic endometrium from women with endometriosis throughout the menstrual cycle by studying bax (pro-apoptotic), c-myc (regulator of cell cycle) and TGF-beta1 (involved in cell differentiation) genes. METHODS: Eutopic endometrium was obtained from: 30 women with endometriosis (32.8 +/- 5 years) and 34 fertile eumenorrheic women (36 +/- 5.3 years). We analyzed apoptosis (TUNEL: DNA fragmentation); cell proliferation (immunohistochemistry (IHC) for Ki67); c-myc, bax and TGF-beta1 mRNA abundance (RT-PCR) and TGF-beta1 protein (IHC) in endometrial explants. RESULTS: Cell proliferation strongly decreased from proliferative to late secretory phases in glands, but not in stroma, in both endometria. Positive staining in glands and stroma from proliferative endometrium with endometriosis was 1.9- and 2.2-fold higher than control endometrium, respectively (p < 0.05). Abundance of c-myc mRNA was 65% higher in proliferative endometrium from endometriosis than normal tissue (p < 0.05). TGF-beta1 (mRNA and protein) augmented during mid secretory phase in normal endometrium, effect not observed in endometrium with endometriosis. In normal endometrium, the percentage of apoptotic epithelial and stromal cells increased more than 30-fold during late secretory phase. In contrast, in endometrium from endometriosis, not only this increase was not observed, besides bax mRNA decreased 63% versus normal endometrium (p < 0.05). At once, in early secretory phase, apoptotic stromal cells increased 10-fold with a concomitant augment of bax mRNA abundance (42%) in endometria from endometriosis (p < 0.05). CONCLUSION: An altered expression of c-myc, TGF-beta1 and bax was observed in eutopic endometrium from endometriosis, suggesting its participation in the regulation of cell survival in this disease. The augmented cell viability in eutopic endometrium from these patients as a consequence of a reduction in cell death by apoptosis, and also an increase in cell proliferation indicates that this condition may facilitate the invasive feature of the endometrium.

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Condition tags

endometriosis

MeSH descriptors

bcl-2-Associated X Protein Cell Survival Endometriosis Proto-Oncogene Proteins c-myc Transforming Growth Factor beta Adult Apoptosis bcl-2-Associated X Protein Cell Proliferation Cell Survival DNA Fragmentation Endometriosis Endometrium Endometrium Endometrium Female Humans Menstrual Cycle Menstrual Cycle Proto-Oncogene Proteins c-myc

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