Amygdalin inhibits endometrial stromal cell proliferation, migration, and invasion in endometriosis mice via inhibiting Wnt/β-catenin signaling

Miaomiao Yu, Lu Yang, Yonghong Pei, Mei Xu
Journal of molecular histology · 2024 · vol. 56(1) , pp. 11 · doi:10.1007/s10735-024-10301-6 · PMID:39612044 · W4404867056
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

Amygdalin reduced endometrial stromal cell proliferation, migration, and invasion in mice by inhibiting Wnt/β-catenin signaling and ectopic lesion growth.

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

This study investigated whether amygdalin affects the proliferation, migration, and invasion of human endometrial stromal cells and examined the role of Wnt/β-catenin signaling in vitro, alongside testing its effects in an induced endometriosis (EMS) mouse model. HESCs were treated with 50, 100, or 200 µg/mL amygdalin, and functional assays showed dose-dependent reductions in “malignant” behaviors; TOP/FOPFlash reporter activity and qRT-PCR demonstrated decreased activation of Wnt/β-catenin signaling, with lower β-catenin, cyclin D1, and c-Myc mRNA levels. In EMS mice, amygdalin progressively inhibited growth of ectopic endometrial lesions. The paper does not state major limitations in the abstract, and data availability indicates no datasets were generated or analyzed during the study. This paper is centrally about endometriosis — it tests amygdalin’s inhibitory effects on endometrial stromal cell invasion and lesion growth via suppression of Wnt/β-catenin signaling in an EMS mouse model.

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Abstract

To explore the impact of amygdalin on the proliferation, migration, and invasion of human endometrial stromal cells (HESCs) and the possible underlying mechanism. HESCs were incubated with 50, 100, and 200 µg/mL of amygdalin. The malignant activities of HESCs were analyzed by functional experiments. The activation of the Wnt/β-catenin signaling was tested using TOP/FOPFlash. The mRNA expressions of genes were validated by qRT-PCR. The endometriosis (EMS) mouse model was induced and the impact of amygdalin on the growth of ectopic endometrial lesions were assessed. It was observed that amygdalin markedly lessened the malignant activities of HESCs in a dose-dependent way (p < 0.05). Amygdalin dose-dependently declined the activation of TOPFlash and mRNA levels of β-catenin, cyclinD1 and c-Myc in HESCs (p < 0.05). Additionally, the increasing dose of amygdalin progressively inhibited the growth of ectopic endometrial lesions in EMS mouse model (p < 0.05). We reached a conclusion that amygdalin could inhibit the malignant activities of HESCs and alleviate EMS, which was related to Wnt/β-catenin signaling activation.

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Condition tags

endometriosis

MeSH descriptors

Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin Amygdalin

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (31)

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