ArticleBiology direct2026
Ovarian cancer-derived ADAMTS2 promotes the omental pre-metastatic niche formation through remodeling collagen I.
Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundEpithelial ovarian cancer (EOC) frequently metastasizes to the omentum, yet the mechanisms driving this site-specific dissemination remain incompletely understood. Through transcriptomic profiling, we previously identified ADAMTS2 (A disintegrin and metalloproteinase with thrombospondin type 1 motifs 2) as the most upregulated gene in highly metastatic EOC (EOC-HM) cells. Here, we investigated the functional role of ADAMTS2 in orchestrating the omental metastatic niche.
resultsIn orthotopic mouse models, silencing ADAMTS2 in EOC-HM cells significantly suppressed spontaneous intraperitoneal metastasis and extended survival. Mechanistically, we observed a negative correlation between tumoral ADAMTS2 expression and omental collagen deposition in both murine models and patient samples, as visualized by polarized picrosirius red staining. Furthermore, EOC-HM cells secreted elevated levels of ADAMTS2 compared to parental lines, and intraperitoneal injection of this ADAMTS2-rich supernatant was sufficient to reduce omental collagen density in vivo. In vitro assays confirmed that ADAMTS2 knockdown impaired the invasive capacity of EOC cells through collagen I matrices and diminished the collagenolytic activity of their conditioned media.
conclusionsThese findings identify tumor-derived ADAMTS2 as a key initiator of extracellular matrix remodeling in the omentum that facilitates subsequent metastatic colonization, providing mechanistic insight into premetastatic niche formation and suggesting ADAMTS2 as a potential therapeutic target in EOC.
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