In vitro models to study novel pathogenesis in therapy for human endometriosis

JIN Miona, KONNO Takumi, KOHNO Takayuki, Kikuchi Shin, KURA Arisa, Arisa Kura, Kimihito Saito, SAITO Kimihito, Shimada Hiroshi, NAGAO Ramu, MATSUURA Motoki, Motoki Matsuura, OHSAKI Yuki, SAITO Tsuyoshi, Saitou Tsuyoshi, KOJIMA Takashi
In: The Sapporo Medical Journal · 2026 · vol. 95 , pp. 65–88 · doi:10.15114/smj.95.65 · W7213633171
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⚙ AI-generated summary by qwen3.7-flash, 2026-10-06 ⓘ

This in vitro study found that TGF-β, activin A, and cytokines promote endometriotic cell migration and permeability, effects prevented by signaling inhibitors and cytokine antibodies.

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⚙ AI-generated deep summary by qwen3.7-flash, 2026-10-02 · read from full text ⓘ

This study utilized in vitro models of human endometrial epithelial cells, stromal cells, and an endometrioid cancer cell line to investigate the pathogenesis of estrogen-dependent chronic disease. Treatments with various growth factors, cytokines, and signaling inhibitors were shown to induce cell migration, invasion, proliferation, and changes in tight junction protein expression, while specific inhibitors and cytokine antibodies prevented these progression-inducing effects. The authors conclude that non-hormonal drugs, signaling inhibitors, and cytokine antibodies can effectively prevent the progression of the condition by blocking these molecular pathways. This paper is centrally about endometriosis — specifically exploring novel therapeutic targets involving cytokine signaling and tight junction regulation in human endometrial cells.

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Abstract

Endometriosis is an estrogen-dependent chronic disease characterized by the growth and migration of endometriotic tissue. Various growth factors, cytokines and tight junction proteins, contribute to the progression of endometriosis; however, the mechanisms underlying the chronic inflammation remain unclear. In the present study, by using in vitro models of human cells, we studied novel pathogenesis, the understanding which might be useful in therapy for endometriosis. We used human endometrial epithelial （HEME） cells and stromal （HEMS） cells derived from endometriotic tissue, and human endometrioid endometrial cancer cell line Sawano. Treatments with the TGF-β family, TGF-β and activin A, an inhibitor of Rho and ROCK inhibitor signaling Y27632, cytokines TNFα, IL-6, IL-17 and IL-22, induced cell migration, invasion, proliferation and metabolism. In some treated HEME and Sawano cells, changes in the expression of tight junction proteins LSR, TRIC and CLDN-1 were observed. Furthermore, in 2.5D cultures of Sawano cells, treatments with activin A, IL-6, IL-17 and IL-22 induced epithelial permeability. The changes induced by all treatments were prevented by not only various signaling inhibitors, MAPK inhibitor U0126, MST1/2 inhibitor XMU-MP-1, proline-rich tyrosine kinase 2 （PYK2） inhibitor PF431396, and glutaminase 1 （GLS1） inhibitor BPTES but also by antibodies for several cytokines, including an anti-IL-6 antibody （siltuximab）, anti-TNFα antibody （infliximab）, and anti-IL-22 antibody （fezakinumab）. Our results suggest that non-hormonal drugs, signaling inhibitors and cytokine antibodies can prevent the progression of human endometriosis.
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WEKO3 アイテム In vitro models to study novel pathogenesis in therapy for human endometriosis https://doi.org/10.15114/smj.95.65 https://doi.org/10.15114/smj.95.65aaa26f8c-68b3-40b2-a5b0-3fb031072210 | 名前 / ファイル | ライセンス | アクション | |---|---|---| | 08_In vitro models to study novel pathogenesis in therapy for human endometriosis.pdf (4.6 MB) | | アイテムタイプ | デフォルトアイテムタイプ（フル）(1) | ||||||||||||||||||||||||||||| |---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---| | 公開日 | 2026-09-15 | ||||||||||||||||||||||||||||| | タイトル | |||||||||||||||||||||||||||||| | タイトル | In vitro models to study novel pathogenesis in therapy for human endometriosis | ||||||||||||||||||||||||||||| | 言語 | en | ||||||||||||||||||||||||||||| | 作成者 | Miona, JIN × Miona, JIN × Takumi, KONNO × Takayuki, KOHNO × Shin, KIKUCHI × Arisa, KURA × Kimihito, SAITO × Hiroshi, SHIMADA × Ramu, NAGAO × Motoki, MATSUURA × Yuki, OHSAKI × Tsuyoshi, SAITO × Takashi, KOJIMA | ||||||||||||||||||||||||||||| | アクセス権 | |||||||||||||||||||||||||||||| | アクセス権 | open access | ||||||||||||||||||||||||||||| | アクセス権URI | http://purl.org/coar/access_right/c_abf2 | ||||||||||||||||||||||||||||| | 主題 | |||||||||||||||||||||||||||||| | 言語 | en | ||||||||||||||||||||||||||||| | 主題 | endometriosis | ||||||||||||||||||||||||||||| | 主題 | |||||||||||||||||||||||||||||| | 言語 | en | ||||||||||||||||||||||||||||| | 主題 | human endometrial epithelial cells | ||||||||||||||||||||||||||||| | 主題 | |||||||||||||||||||||||||||||| | 言語 | en | ||||||||||||||||||||||||||||| | 主題 | human endometrial stromal cells | ||||||||||||||||||||||||||||| | 主題 | |||||||||||||||||||||||||||||| | 言語 | en | ||||||||||||||||||||||||||||| | 主題 | tight junctions | ||||||||||||||||||||||||||||| | 内容記述 | |||||||||||||||||||||||||||||| | 内容記述タイプ | Abstract | ||||||||||||||||||||||||||||| | 内容記述 | Endometriosis is an estrogen-dependent chronic disease characterized by the growth and migration of endometriotic tissue. Various growth factors, cytokines and tight junction proteins, contribute to the progression of endometriosis; however, the mechanisms underlying the chronic inflammation remain unclear. In the present study, by using in vitro models of human cells, we studied novel pathogenesis, the understanding which might be useful in therapy for endometriosis. We used human endometrial epithelial （HEME） cells and stromal （HEMS） cells derived from endometriotic tissue, and human endometrioid endometrial cancer cell line Sawano. Treatments with the TGF-β family, TGF-β and activin A, an inhibitor of Rho and ROCK inhibitor signaling Y27632, cytokines TNFα, IL-6, IL-17 and IL-22, induced cell migration, invasion, proliferation and metabolism. In some treated HEME and Sawano cells, changes in the expression of tight junction proteins LSR, TRIC and CLDN-1 were observed. Furthermore, in 2.5D cultures of Sawano cells, treatments with activin A, IL-6, IL-17 and IL-22 induced epithelial permeability. The changes induced by all treatments were prevented by not only various signaling inhibitors, MAPK inhibitor U0126, MST1/2 inhibitor XMU-MP-1, proline-rich tyrosine kinase 2 （PYK2） inhibitor PF431396, and glutaminase 1 （GLS1） inhibitor BPTES but also by antibodies for several cytokines, including an anti-IL-6 antibody （siltuximab）, anti-TNFα antibody （infliximab）, and anti-IL-22 antibody （fezakinumab）. Our results suggest that non-hormonal drugs, signaling inhibitors and cytokine antibodies can prevent the progression of human endometriosis. | ||||||||||||||||||||||||||||| | 言語 | en | ||||||||||||||||||||||||||||| | 出版者 | |||||||||||||||||||||||||||||| | 出版者 | 札幌医科大学 | ||||||||||||||||||||||||||||| | 言語 | ja | ||||||||||||||||||||||||||||| | 言語 | |||||||||||||||||||||||||||||| | 言語 | eng | ||||||||||||||||||||||||||||| | 資源タイプ | |||||||||||||||||||||||||||||| | 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | ||||||||||||||||||||||||||||| | 資源タイプ | departmental bulletin paper | ||||||||||||||||||||||||||||| | 出版タイプ | |||||||||||||||||||||||||||||| | 出版タイプ | VoR | ||||||||||||||||||||||||||||| | 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | ||||||||||||||||||||||||||||| | ID登録 | |||||||||||||||||||||||||||||| | ID登録 | 10.15114/smj.95.65 | ||||||||||||||||||||||||||||| | ID登録タイプ | JaLC | ||||||||||||||||||||||||||||| | 収録物識別子 | |||||||||||||||||||||||||||||| | 収録物識別子タイプ | EISSN | ||||||||||||||||||||||||||||| | 収録物識別子 | 2759-8349 | ||||||||||||||||||||||||||||| | 書誌情報 | ja : 札幌医学雑誌 en : The Sapporo Medical Journal 巻 95, p. 65-88, ページ数 24, 発行日 2026-09-30 |

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