Disrupting Y-Box-Binding Protein 1 Function Using OSU-03012 Prevents Endometriosis Progression in In Vitro and In Vivo Models

Cássia G T Silveira, Gabriele Marschner, Geraldine O Canny, Silke Klocke, Peter Hunold, Frank Köster, Thorben Ahrens, Achim Rody, Daniela Hornung
Reproductive sciences (Thousand Oaks, Calif.) · 2017 · doi:10.1177/1933719116649695 · PMID:27217374
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

The novel celecoxib derivative OSU-03012, by disrupting Y-box-binding protein 1 function, reduced endometriotic lesion size and epithelial cell proliferation in vitro and in vivo mouse models.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 · read from full text ⓘ

The study evaluated whether OSU-03012, a celecoxib-derivative designed to indirectly block Y-box-binding protein 1 (YB-1) function, could impair endometriosis progression. 12Z human endometriotic epithelial cells and sexually mature female C57BL/6J mice were treated with OSU-03012, with proliferation assessed by MTT assay and YB-1 and phosphorylated YB-1 measured by Western blotting and immunohistochemistry, including Ki-67/IHC for proliferating cell nuclear antigen. OSU-03012 reduced YB-1 and phosphorylated YB-1 in vitro and in endometriotic lesions, and significantly decreased lesion size in mice and epithelial cell proliferation within lesions. A key caveat is that conclusions rely on these in vitro and mouse model systems rather than direct human validation. This paper is centrally about endometriosis — it tests OSU-03012–mediated YB-1 disruption to prevent endometriosis progression in in vitro and in vivo models.

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Abstract

The objective of the present study was to test the ability of OSU-03012 (2-amino-N-[4-[5-phenanthren-2-yl-3-(trifluoromethyl)pyrazol-1-yl]phenyl]acetamide), a novel and potent celecoxib-derivative, to impair endometriosis progression in in vitro and in vivo models based on its ability to indirectly block Y-box-binding protein 1 (YB-1) function. 12Z human endometriotic epithelial cells and sexually mature female C57BL/6J mice were treated with OSU-03012. Cellular proliferation was quantified by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromid assay. Expression of YB-1 and phosphorylated YB-1 in 12Z cells and endometriotic lesions was evaluated by Western blotting and immunohistochemistry (IHC). The IHC for proliferating cell nuclear antigen was performed. OSU-03012 treatment resulted in decreased YB-1 and its phosphorylated form in both in vitro and in vivo models. Endometriotic lesion size was significantly reduced in OSU-03012-treated mice (27.6 ± 4.0 mm3) compared to those from the control group (50.5 ± 6.9 mm3, P < .0001). A significant reduction in endometriotic epithelial cell proliferation was observed in endometriotic lesions exposed to OSU-03012 treatment ( P = .0346). In conclusion, targeting YB-1 via OSU-03012 showed a potent antiproliferative effect on endometriotic epithelial cells in vitro and in a mouse model of disease.
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Disrupting Y-Box-Binding Protein 1 Function Using OSU-03012 Prevents Endometriosis Progression in In Vitro and In Vivo Models The objective of the present study was to test the ability of OSU-03012 (2-amino-N-[4-[5-phenanthren-2-yl-3-(trifluoromethyl)pyrazol-1-yl]phenyl]acetamide), a novel and potent celecoxib-derivative, to impair endometriosis progression in in vitro and in vivo models based on its ability to indirectly block Y-box-binding protein 1 (YB-1) function. 12Z human endometriotic epithelial cells and sexually mature female C57BL/6J mice were treated with OSU-03012. Cellular proliferation was quantified by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromid assay. Expression of YB-1 and phosphorylated YB-1 in 12Z cells and endometriotic lesions was evaluated by Western blotting and immunohistochemistry (IHC). The IHC for proliferating cell nuclear antigen was performed. OSU-03012 treatment resulted in decreased YB-1 and its phosphorylated form in both in vitro and in vivo models. Endometriotic lesion size was significantly reduced in OSU-03012-treated mice (27.6 +/- 4.0 mm(3)) compared to those from the control group (50.5 +/- 6.9 mm(3), P < .0001). A significant reduction in endometriotic epithelial cell proliferation was observed in endometriotic lesions exposed to OSU-03012 treatment (P = .0346). In conclusion, targeting YB-1 via OSU-03012 showed a potent antiproliferative effect on endometriotic epithelial cells in vitro and in a mouse model of disease. WOS:000393666600007 2017 24 1 67 76 REVIEWED EPFL

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