Effects of an inhibitor of the SHH signaling pathway on endometrial cells of patients with endometriosis

Yanan He, Jing-kai Wang, J Wang, Xinyan Jiang, Jianhua Gao, Yan Cheng, Tian Liang, Jun Zhou, Liyuan Sun, Guangmei Zhang
BMC molecular and cell biology · 2022 · vol. 23(1) , pp. 37 · doi:10.1186/s12860-022-00426-5 · PMID:35933378 · W4290034024
article OA: gold CC0 ⤵ 4 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated the SHH signaling pathway in endometriosis, finding that its inhibition by GANT61 reduced endometrial stromal cell proliferation and invasion in vitro and in vivo.

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

This study examined whether inhibiting the Sonic Hedgehog (SHH) signaling pathway affects endometrial stromal cells (ESCs) derived from eutopic endometrium of women with or without endometriosis, using cell isolation/culture, immunofluorescence to identify ESC purity, and in vitro assays for proliferation, migration, and invasion after treatment with the GLI inhibitor GANT61. GANT61 at higher concentrations reduced ESC proliferation and migration distance and inhibited invasion, with SHH pathway blockade significantly reducing proliferation in vitro. The main caveat is that the work relies on in vitro functional assays using a relatively small number of patient-derived samples and relies on experimental cell models rather than direct mechanistic confirmation beyond pathway inhibition. This paper is centrally about endometriosis—testing how SHH/GLI inhibition in endometrial stromal cells impacts proliferation, migration, and invasion relevant to endometriosis pathogenesis.

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Abstract

BACKGROUND: Endometriosis is one of the most common gynecological diseases, and seriously reduces the quality of life of patients. However, the pathogenesis of this disease is unclear. Therefore, more studies are needed to elucidate its pathogenesis. Our previous publication found that the Sonic Hedgehog (SHH) signaling pathway was activated in endometriosis. This study tested whether SHH signaling in endometrial stromal cells (ESCs) was critical for the pathogenesis of endometriosis. METHODS: To examine the effect of inhibiting the SHH signaling pathway on endometriosis, we first isolated ESCs from eutopic endometrial tissues of patients with or without endometriosis and identified the extracted cells by morphological observation and immunofluorescence. Then, we treated ESCs with the GLI inhibitor GANT61 and used CCK-8, wound healing and invasion assays to detect cell activities, such as proliferation, invasion and metastasis. Furthermore, we detected the expression of key proteins and proliferation markers of the SHH signaling pathway in the lesions of nude mice using immunochemistry. RESULTS: We demonstrated that higher concentrations of GANT61 decreased the proliferation rate and migration distance of ESCs. We observed that GANT61 inhibited the invasion of ESCs. In addition, blockage of the SHH signaling pathway significantly reduced cell proliferation in vitro. CONCLUSIONS: Our study suggested that inhibition of the SHH pathway is involved in cell proliferation and invasive growth in the pathogenesis of endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Animals Animals Animals Animals Female Female Female Female Hedgehog Proteins Hedgehog Proteins Hedgehog Proteins Hedgehog Proteins Humans Humans

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